AGE DISTRIBUTION

PREVALENCE, ETIOLOGY , CLINICAL PROFILE AND OUTCOME OF ACUTE KIDNEY INJURY IN A TERTIARY CARE

HOSPITAL

DISSERTATION SUBMITTED TO THE TAMILNADU DR.M.G.R. MEDICAL UNIVERSITY, CHENNAI In partial fulfilment of the requirements for the degree of

M.D. BRANCH – I (GENERAL MEDICINE) Registration No.: 201711363

DEPARTMENT OF GENERAL MEDICINE TIRUNELVELI MEDICAL COLLEGE HOSPITAL

TIRUNELVELI – 627011

BONAFIDE CERTIFICATE

This is to certify that the dissertation entitled PREVALENCE, ETIOLOGY, CLINICAL PROFILE AND OUTCOME OF ACUTE KIDNEY INJURY IN A TERTIARY CARE HOSPITAL submitted by Dr.

S.POORNIMA to the Tamilnadu Dr. M.G.R Medical University, Chennai, in partial fulfillment of the requirement for the award of M.D. Degree Branch – I (General Medicine) is a bonafide research work carried out by her under direct supervision & guidance.

Professor & Head of the Department,

Department of General Medicine Tirunelveli Medical College,

Tirunelveli.

Unit Chief,

Department of General Medicine Tirunelveli Medical College,

Tirunelveli.

CERTIFICATE BY THE DEAN

I hereby certify that this dissertation entitled PREVELANCE, ETIOLOGY ,CLINICAL PROFILE AND OUTCOME OF ACUTE KIDNEY INJURY IN A TERTIARY CARE HOSPITALis a record of work done by Dr. S.POORNIMA in the Department of General Medicine, Tirunelveli Medical College, Tirunelveli, during her postgraduate degree course period from 2017- 2020. This work has not formed the basis for previous award of any degree.

Date :

Place : TIRUNELVELI The DEAN

Tirunelveli Medical College, Tirunelveli - 627011.

DECLARATION

I solemnly declare that the dissertation entitled PREVALENCE, ETIOLOGY,CLINICAL PROFILE AND OUTCOME OF ACUTE KIDNEY INJURY IN A TERTIARY CARE HOSPITAL is done by me at Tirunelveli Medical College Hospital, Tirunelveli Under the guidance and supervision ofProf.Dr.Ravichandran M.D, the dissertation is submitted to The Tamilnadu Dr. M.G.R. Medical University towards the partial fulfilment of requirements for the award of M.D. Degree (Branch I) in General Medicine.

Place: Tirunelveli

Date: Dr.S.POORNIMA

Registration No.: 201711363 Postgraduate Student, M.D General Medicine, Department of General Medicine,

Tirunelveli Medical College Tirunelveli.

CERTIFICATE – II

This is to certify that this dissertation work entitled PREVALENCE, ETIOLOGY,CLINICAL PROFILE AND OUTCOME OF ACUTE KIDNEY INJURY IN A TERTIARY CARE HOSPITAL of the candidate Dr.R.S.POORNIMA with registration Number 201711363 for the award of M.D.Degreein the branch of GENERAL MEDICINE (I).I personally verified the urkund.com website for the purpose of plagiarism check. I found that the uploaded thesis file contains from introduction to conclusion page and result shows3 percentageof plagiarism in the dissertation.

Guide & Supervisor sign with Seal.

ACKNOWLEDGEMENT

I wish to express my heartfelt gratitude to our Dean Prof.Dr. S. M. .Kannan M.S., MCh., Tirunelveli Medical College for allowing me to do the study in this institution.

I would like to express my humble thanks to our professor & Head of the Department Prof .Dr .M.Ravichandran M.D., Department of General Medicine.

I express my sincere thanks to my renowned teacher and my guide Dr.G..M.Ravichandran M.D., Professor, Department of General Medicine, Tirunelveli Medical College for his guidance, valuable suggestions and constant encouragement throughout the study.

I express my sincere thanks to my former professor, Dr.S.Arumugapandian

@ Mohan, M.D., for his constant support, encouragement and suggestions which helped me greatly to expedite this dissertation .

I am greatly obliged to Prof.Dr.Ramsubramaniam M.D, D.M(Nephrology), Dr.P.K.Senthilkumar M.D, D.M (Nephrology), Dr.Thomas Kinsley M.D, Dr.Rajesh Babu M.D, Dr Bobby M.D.D.M (Neurology) Dr.Narayanan M.D., and Assistant Professors, Dept .of General Medicine for their valuable suggestions in preparing this dissertation.

CONTENT

S.NO TITLE PAGE.NO

1. INTRODUCTION 1

2. AIM AND OBJECTIVES OF THE STUDY 2

3. REVIEW OF LITERATURE 4

4. MATERIALS AND METHODS 47

5. RESULTS 50

6. DISCUSSION 88

8. CONCLUSION 91

9. LIMITATIONS OF THE STUDY 92

10. BIBILIOGRAPHY 11. MASTER CHART

LIST OF ABBREVIATIONS:

AKI - Acute Kidney Injury

ACE-I – Angiotensin Converting Enzyme Inhibitors

AGE - acute gastroenteritis

AGN - Acute Glomerulo Nephritis

ANCA - Anti Cytoplasmic Antibody

ANA - Anti Nuclear Antibody

ATN - Acute Tubular Necrosis

BOO - Bladder Outlet Obstruction

BUN - Blood Urea Nitrogen

CAPD - Continous Amubulatory Peritoneal Dialysis CCPD - Continous Cyclical Peritonea Dialysis CIN - Contrast Induced Nephropathy

CKD - Chronic Kidney Disease

CRRT - Continous Renal Replacement Therapy CVVHDF - Continous Veno-Venous HemoDiaFiltration

ESRD - End Stage Renal Disease

FeNA - Fractional excretion of sodium IGF-1 - Insulin like Growth Factor 1

IGFBP-7 - (Insulin Like Growth Factor Binding Protein 7)

IHD - Intermittent Hemodialysis

NAG - N Acteyl d-Glucosaminidase

NGAL - Neutrophil Gelatinase Associated Lipoprotein

RPGN - Rapidly Progressive Renal Failure SLED - Sustained Low Efficacy Dialysis UF - Ultra Filtration

URR - Urine Reduction Ratio

INTRODUCTION

Acute kidney injury (AKI) is characterized by rapid decline in GFR (Glomerular Filtration Rate)- hours to days because of retention of nitrogenous waste products and perturbation of extracellular volume and fluid, alteration in electrolyte & acid base homeostasis. It is important to recognize AKI as a clinical diagnosis and not a structured one. A patient may have AKI without injury to renal parenchyma. The term acute renal failure is replaced by acute kidney injury (AKI). there is paucity of data on the incidence and profile of AKI in hospitalized patients from the developing world

Previously acute loss of renal function is termed as acute renal failure been modified to acute kidney injury. The term AKI was introduced by Acute Dialysis Quality Initiative (ADQI).

Acute kidney injury may range in severity from asymptomatic &

transient changes in laboratory parameters of GFR to overwhelming and rapidly fatal derangements in effective circulating volume regulation, electrolyte and acid base composition of the plasma. Detection of AKI in its early and potentially reversible stages to prevent its progression to chronic kidney disease is of paramount importance. AKI is amenable to early detection and potential prevention. AKI is suspected when biochemical monitoring of hospitalized patients reveal a new increase in blood urea and serum creatinine levels.

Relatively small changes in renal function can cause short & long term clinical outcomes. AKI can occur in a wide variety of settings including ambulatory ,outpatient, hospitalized & critically ill patients. Kidneys have the ability to recover from almost complete loss of function.

After an episode of AKI , recovery of renal function occurs in majority of the patients , some become dialysis dependent with severe renal impairment.

Recently it has been recognized that even patients who have complete/ near complete recovery of renal functions are at increased risk of CKD and superimposition of AKI on CKD is associated with accelerated progression to ESRD.

AIMS AND OBJECTIVES

1. To evaluate the prevalence of AKI

2. To identify the causes of AKI

3. To evaluate the clinical profile of AKI and

4. To assess the complications and outcome associated with AKI in patients admitted to Tirunelveli Medical College.

REVIEW OF LITERATURE

HISTORICAL REVIEW

In 1888, microscopic pathology of acute kidney injury as described by DALAFIELD.

During World War 1, the term ‘War Nephritis’ (AKI due to trauma) introduced

In 1941, Waters and Bralls in World War 2, demonstrated tubular damage and pigment cast in the tubules in crush victims with impaired renal function in tied LANDMARK ARTICLE.

In 1951, term acute renal failure was used in the book ‘THE KIDNEY STRUCTURE AND FUNCTION IN HEALTH SCIENCE by HORMER W SMITH’ .

In 1967, hemodialysis was introduced by Silverstein Lee Henderson.

In 1979, continous AV Hemodialysis was demonstrated by Kraner.

The term acute renal failure was replaced as acute kidney injury in 2004.

HISTORICAL MILESTONES

GALEN (EMPTY BLADDER)

(ISCHURIA RENALIS)- (18 TH CENTURY) MORGAGNI

(ACUTE BRIGHTS DISEASE)- (19 TH CENTURY) -BRIGHT

1917(WAR NEPHRITIS)- DAVIES

1941(CRUSH SYNDROME)- BYWATERS AND BAELL,

1951 (ACUTE RENAL FAILURE)-SMITH

ACUTE DIALYSIS QUALITY INITIATIVE ,2004 (ACUTE KIDNEY INJURY)

DEFINITION AND STAGING OF AKI:

 It is defined by one of the following (KDIGO)

 Increase in serum creatinine by more than or equal to 0.3 mg/dl within 48 hour

 Increase in serum creatinine by more than or equal to 1.5 times from baseline which is presumed to have occurred within the previous seven days

 Urine volume <0.5 ml/kg/hr for more than six hours

EPIDEMIOLOGY:

AKI complicates 5-7% of acute care hospital admissions and upto 30 % of admission to intensive care unit. In India acute kidney injury constitutes 1.5% all general hospital admissions of which 60 % are due to medical causes, most common causes are acute diarroheal diseases, sepsis, infection, malaria, urinary tract infections, pneumonia, viral hepatitis, snake bite, cardiac failure, renal failure, Diabetes mellitus, nephrotoxic drugs, malignancy , hypertension, major surgery like whipples procedure. Advanced age, liver diseases, underlying comorbid illness (diabetes mellitus/hypertension/ischemic heart disease/chronic obstructive pulmonary disease & cirrhosis) have been implicated as a risk factor for the development of AKI. AKI increases the risk for the development or worsening of chronic kidney disease(AKI). Patients who

requiring end stage kidney disease. AKI is major medical complication in the developing world ,where the epidemiology differs from the developing countries due to differences in demographics, economics, environmental factors and comorbid disease burden.

The pathophysiology of AKI leads to increased hydrostatic pressure in renal tubules and decreased GFR. Inspite of recent advances in renal replacement therapy, mortality due to AKI is high. Poor prognostic factors of AKI are Age

>65 years, Acute Respiratory Distress Syndrome, Multi organ dysfunction syndrome.

CAUSES OF AKI:

AKI can be community acquired or hospital acquired.

Community acquired AKI causes- volume depletion

heart failure

adverse effects of medications

obstruction to urinary tract

malignancy

Hospital acquired AKI causes - sepsis

major surgical procedures

heart or liver failure

nephrotoxic medications

AKI is divided into three categories:

1.Diseases characterized by renal hypoperfusion where integrity of renal parenchyma is preserved (Prerenal)

2.Diseases involving renal parenchyma (Intrinsic)

3.Diseases involving urinary tract obstruction (Postrenal)

AKI is often reversible, but it can lead to significant irreversible damage that leads to chronic kidney disease with associated in hospital morbidity & mortality based on the presence or absence of non renal organ dysfunction. There is a lack of a uniform clinical presentation with variation in nature of injury. AKI can be oliguric or non oliguric which depends upon daily urine excretion which has got a prognostic significance.

OLIGURIA-urine output less than 400 ml/day.

ANURIA-urine output less than 100 ml/day, abrupt onset suggests bilateral obstruction and catastrophic injury to both kidneys.

ETIOLOGY AND PATHOPHYSIOLOGY:

PRERENAL-adaptive response to severe volume depletion & hypotension, with structurally intact nephrons

INTRINSIC: occurs in response to ischemic, cytotoxic or inflammatory insult to the kidney, with structural and functional organ damage.

POSTRENAL: arises due to obstruction to outflow of urine.

CAUSES OF PRERENAL AKI:

HYPOVOLEMIA:

INCREASED EXTRACELLULAR FLUID LOSS:

Gastrointestinal fluid loss (diarrhoea, vomiting), hemorrhage, renal fluid loss, nephrogenic diabestes insipidus, hypoadrenalism, osmotic diuresis.

REDUCED INTAKE:

Altered mental status, hypovolemia,

EXTRAVASCULAR SEQUESTRATION:

Burns, severe hypoproteinemia, pancreatitis

LOW CARDIAC OUTPUT STATE:

 Pericardial diseases (cardiac tamponade)

 Diseases of the myocardium or valves

 Impaired venous return (positive pressure ventilation or abdominal compartment syndrome)

 Pulmonary hypertension

 Massive pulmonary embolism

RENAL VASOCONSTRICTION:

 Hypocalcemis

 Calcineurin inhibitors

 Catecholamine

 Amphotericin B

SYSTEMIC VASODILATATION

 Sepsis

 Antihypertensive

 Anaphylaxis

IMPAIRED RENAL AUTOREGULATION:

 Cyclooxygenase inhibitors

 Angiotensin converting enzyme inhibitors

 Hepatorenal syndrome

Hypotension and altered hemodynamics- hemorrhage, vasodilation and increased vascular permeability.

PRERENAL AZOTEMIA:

Prerenal azotemia (azo meaning nitrogen; emia meaning in the blood) is the most commom form of AKI.

By definition prerenal azotemia involves no parenchymal damage to the kidney and it is rapidly reversible once intraglomerular hemodyanamics and parenchymal blood flow is restored. The common clinical conditions associated

renal autoregulatory responses such as non steroidal anti-inflammatory drugs (NSAIDS) and inhibitors of angiotensin 2.

It is caused due to inadequate plasma flow with rise in blood urea and serum creatinine. Prerenal azotemia may coexist with other forms of intrinsic AKI with processes affecting directly the renal parenchyma.

Prerenal AKI represents the most common of kidney injury and leads to intrinsic AKI if not promptly treated. Volume loss from gastrointestinal tract, renal, burns, hemorrhage can cause AKI. It is caused due to decreased renal perfusion.

PATHOPHYSIOLOGY:

In prerenal AKI, restoration of normal renal perfusion results in early recovery of renal function but sustained renal hypoperfusion results in irreversible renal injury. Arterial blood volume depletion or decreased renal perfusion is explained by activation of renin angiotensin system and sympathetic nervous system.

Increased angiotension 2 level causes constriction of preglomerular and postglomerular arterioles (predominance of which maintain intraglomerualr capillary pressure to normal and maintains normal GFR) which is opposed by vasodilator prostaglandins.

Hemodyanamic factors, sympathetic nervous system activation, increased levesl of angiotensin 2, will increase proximal tubular sodium and water reabsorption. In prerenal AKI, the regulatory mechanisms are unable to compensate fully for more severe degrees of hypoperfusion ,which leads to decline in glomerular filtration rate. Autoregulation is the first line of defence by kidney against fluctuations in arterial blood pressure. When renal perfusion decreases, the afferent arteriole senses the degree of stretch and thus relaxes.

This is called“myogenic reflex”.

TUBULO-GLOMERULAR FEEDBACK:

Also plays an important role in autoregulation. Macula densa presenting in the cortical collecting ducts senses the decrease in solute delivery to the distal tubules and leads to dilatation of afferent arteriole by nitic oxide release.

AUTOREGULATION:

Decrease in renal perfusion

Renin , angiotensin 2 prostaglandins

increased efferent arteriole tone decreased efferent arteriole tone

maintained GFR

Autoregulation and other intrinsic compensatory mechanisms fails once the systolic blood pressure falls below 80 mm hg.

FAILURE OF AUTOREGULATION:

Decreased renal perfusion

renin , angiotensin 2 prostaglandins

ACE inhibitors NSAIDS

decreased efferent arteriolar tone increased afferent arteriole tone

reduced GFR

CAUSES OF INTRINSIC AKI:

The hallmark of intrinsic AKI is structural injury in the kidney Acute tubular injury (ATN), ischemic or cytotoxic is the most common form. Frank necrosis is not obvious in most cases, it can be patchy. These changes are predominately observed in glomeruli.

RENOVASCULAR CAUSES: (bilateral/unilateral in the setting of one kidney)

• Atherosclerotic plaque

• Large vessel vasculitis

• Dissecting aneurysm

• Thrombosis

• Embolism

• Obstruction of renal vein –thrombosis and compression

DISEASES OF GLOMERULAR VASCULATURE:

• Glomerulonephritis

• Disseminated intravascular coagulation

• Thrombotic microangiopathy

• Collagen vascular diseases (systemic lupus erythematosus, scleroderma)

• Malignant hypertension

ACUTE TUBULAR NECROSIS (ATN):

Ischemia-causes are the same as for prerenal, but generally the effect is more severe.

TOXINS-EXOGENOUS:

Calcineurin inhibitors, antibiotics (aminoglycosides,radiocontrast), antifungals (amphotericin b, ethylene glycol), chemotherapy (cisplatin)

ENDOGENOUS -(rhabdomyolysis, hemolysis)

ACUTE INTERSTITIAL NEPHRITIS:

Allergic: Antibiotics (beta lactams, sulfonamides, quinolones, rifampicin, NSAID, diuretics)

Infiltration: lymphoma, leukemia, sarcoidosis

Infection: pyelonephritis

Inflammatory: sjogrens disease

Tubulointerstitial:nephritis with uveitis

Intratubular obstruction: Endogenous-Myeloma proteins

Uric acid (tumour lysis syndrome)

Systemic oxalosis

Exogenous-Acyclovir, ganciclovir, indinavir, methotrexate

ACUTE TUBULAR NECROSIS:

Acute tubular necrosis is multifactorial due to sepsis, hyponatremia, nephrotoxic drugs. Clinically ATN has initially oliguric phase within 24 hours of insult and last for 1-3 weeks followed by diuretic phase indicating renal recovery. Complete recovery may not occur.

Urine sediment has muddy brown granular cast.

FeNa >30%

Urinary sodium>40 mmol/litre

Granular cast is formed due to sloughing of cells.

ISCHEMIC ATN:

Desquamation of tubular cells

Vasoconstriction

Production of inflammatory mediators ends in interstitial inflammation

Intraluminar tubular obstruction leads to tubular backleak

Local ischemia and small vessel obstruction

NEPHROTOXIC ATN:

Mechanism Agent

Direct tubular injury Aminoglycosides, vancomycin, cisplatin, cyclosporine, foscarnet, heavy metals, radiocontrast agents, amphotericin B

Endothelial cell injury

Quinine, tacrolimus, cyclosporin, cocaine, mitomycin

Efferent arteriolar vasoconstriction

Angiotensin Converting enzyme inhibitors

Interstitial nephritis Any drug

Vasoconstriction NSAIDS, cyclosporine, radiocontrast, heme pigments, amphotericin B

Hemolytic uremic syndrome

Mitomycin ,conjugated estrogen, quinine, cocaine, tacrolimus, cyclosporine

Crystalluria Sulfonmaides, ethylene glycol, methotrexate, triamterene, uric acid, protease inhibitors, acyclovir Glomerulopatathy NSAIDS, gold, penicillamine

ACUTE GLOMERULONEPHRITIS (AGN):

Pathology is damage to glomerular basement membrane and glomerular bleeding.

AGN and RPGN–

 Most common causes are post streptococcal glomerulonephritis, infections and endocarditis.

 Urine shows RBC casts and dysmorphic RBC

 Serology- complement assay ,Hepatitis B ,Hepatitis C, Anti-streptococcal antibody, anti-GBM antibody, ANA.

 RENAL BIOPSY –proliferative changes in glomerulus and crescent formation.

ACUTE INTERSITIAL NEPHRITIS:

 Occurs due to lymphocytic infiltration of intersitium.

 Causes are infection, antibiotics, NSAIDS, malignancy, and systemic disease. and presents as fever, rash, eosinophilia, eosinophiluria.

 Urine findings: sterile pyuria, haematuria , WBC casts, non-neprotic range of proteinuria.

 Renal biopsy is diagnostic.

SEPTIC ACUTE TUBULAR NECROSIS:

 Endotoxins

 Microvascular endothelial damage

 Systemic and renal hypoperfusion

 Inflammatory mediators activation

CONTRAST INDUCED NEPHROPATHY (CIN):

 Rapid decline in renal function after radiocontrast administration.

 Serum creatinine raises 24-72 hours after contrast administration and peaks at 3-5 days and returns to baseline within 3-5 days.

AKI DUE TO ACUTE GASTROENTERITIS:

Occurs commonly in children and elderly. Renal hypoperfusion is caused due to severe diarrhoea with fluid and electrolye loss with associated renal vasoconstriction. Epithelial cell shedding with tubular dysfunction seen.

Clinical features are hypokalemia, oliguria, bicarbonate loss causing metabolic acidosis.can lead to metabolic encephalopathy. Mortality occurs due to hypovolemic shock and late referral.

Study done by Chugh et al demonstrated earlier treatment , improving sanitary measures and handwashing reduces post diarrhoeal AKI to <10% from 23%.

SNAKE BITE INDUCED AKI:

 DIAGNOSTIC CRITERIA- GFR<60 ml/min/1.73 m² within 72 hours after snake bite.

 Snake bite induced AKI is increased in the following group of patients- deranged hemodyanamic profile, an abnormal whole blood clotting time (WBCT), prothrombin time/activated partial thromboplastin time above 1.5 times the normal.

 Blood parameters-crenated red blood cells in peripheral smear, increase in serum creatinine >30% from baseline, proteinuria, raised D dimer.

 Platelets<1 lakh/cubic mm of blood.

FEVER INDUCED AKI:

 Common in malarial infection

 Incidence in endemic area being >4% with 45% mortality rates.

 Parasitized red cells causing impaired microcirculation is the pathogenesis. Other causes are intravascular hemolysis, disseminated intravascular coagulation(DIC), jaundice and hypovolemia.

 Panda et all study demonstrated that 20% of the patients with malaria developed

AKI IN INDIA: Common causes are

 Sepsis

 Acute gastroenteritis

 Nosocomial

 Nephrotoxic drug induced

 Fever- malaria, viral haemorrhagic fever, leptospirosis

PIGMENT NEPHROPATHY:

 Hemoglobinuria after hemolysis

 Myoglobinuria after rhabdomyolysis

CAUSES OF POSTRENAL AKI:

UPPER URINARY TRACT OBSTRUCTION:

INTRINSIC- Nephrolithiasis

Papillary necrosis

Blood clots

Transitional cell carcinoma

EXTRINSIC- Retroperitoneal adenopathy/fibrosis

Retroperitoneal /pelvic malignancy

Abdominal aortic aneurysm

Endometritis

LOWER URINARY TRACT OBSTRUCTION:

BLADDER- Neurogenic bladder

Transitional cell carcinoma

Bladder calculus

Benign prostatic hypertrophy

Prostate cancer

Blood clot

URETHRA- Stictures

Phimosis

Urethral valves

CLINICAL COURSE OF AKI:

Characterized by three phases:

INITIATION PHASE (HOURS TO DAYS)

Initial period of renal hypoperfusion, during which ischemic injury is evolving. GFR declines due to backleak of glomerualr filtrate through injured tubular lumen, reduction in glomerualr ultrafiltaration rate and presence of glomerular filtrate within the tubules.

Restoration of renal perfusion or elimination of nephrotoxin may recover or limit the kidney injury.

MAINTANENCE PHASE:

Phase of established renal inury. Lasts for one to two weeks. Urine output will be low. GFR stablises at nadir (5 to 10 ml/min).

RECOVERY PHASE:

Characterized by repair and regeneration of renal parenchymal cells. The recovery phase may be complicated by diuretic phase with excretion of salt and water. Recovery of renal function will be better for young when compared to older people. Sodium handling and concentration function are the last to recover.

CLINICAL FEATURES OF ACUTE KIDNEY INJURY:

The common symptoms are:

 Oliguria-urine output less than 400 ml/day

 Anuria

 Breathlessness

 Nausea and vomiting

 Convulsion

 Obstructive urinary symptoms

 Weakness

Physical signs:

PRERENAL AKI:

• Postural hypotension

• Low jugular venous pressure

• Decreased effective circulatory volume-heart failure, hepatic failure

• Dry mucous membrane

INTRINSIC RENAL FAILURE:

• Renal artery thrombosis-abdominal pain /flank pain

• Hemolytic uremic syndrome- fever, neurological abnormalities

• Malignant hypertension- features of end organ damage like blurring of vision, headache, left ventricular hypertrophy , heart failure

• Exogenous toxins-exposure to nephrotoxic antibiotics, or chemotherapy or radiotherapy

• Small vessel vasculitis and glomeruli- new onset cardiac murmur (postinfectious), lung hemorrhage (anti GBM, ANCA, lupus), skin ulcers and rashes (lupus), sinusitis (anti –GBM disease).

• Endogenous toxins- rhabdomyolysis (prolonged immobilization, trauma, post-ictal state), hemolysis (following blood transfusion)

• Ischemia- recent hemorrhage, hypotension

• Multiple myeloma-age more than 60 years, fatiguability, malaise, low back ache

• Ethylene glycol (alcohol abuse, altered mental status).

POSTRENAL AKI:

• Recurrent urinary tract infection and renal calculi

• Anuria and pyuria

• Increased urinary frequency and urgency

• Dysuria

• Urinary dribbling

• Prostate, cervical , retroperitoneal, intrabdominal or pelvic tumours

• Prior radiation therapy to abdomen of vaginal bleeding, subtotal hysterectomy.

COMPLICATIONS OF AKI:

• Hypervolemia & hypovolemia

• Uremia

• Infections

• Hyponatremia

• Bleeding

• Acidosis

• Hyponatremia

• Acidosis

• Bleeding

• Malnutrition

• Cardiac complications like pericardial effusion, pericarditis and arrthymias

LABORATORY INDICES OF AKI:

• Complete blood count – hemoglobin, platelets, total count and erythrocyte sedimentation rate (ESR)

• Renal function tests- blood urea, serum creatinine

• Serum electrolytes

• Liver function tests

• Peripheral smear for malarial parasites

• Serology for IgM leptospirosis

INDICATORS FOR DIAGNOSIS:

• Renal artery thrombosis presents with elevated LDH

• Prerenal AKI -elevated BUN/ creatinine values>20% is diagnostic

• Decreased complement levels with eosinophilisa in atheroembolism

• Peripheral smear with schistocytes raised LDH, thrombocytopenia with anemia in hemolytic uremic syndrome

• Hypocomplementemia, anti- glomerular basement antibody ,ANA,

• Raised myoglobin and creatinine kinase in rhabdomyolysis

• Metabolic acidosis with high anion gap in ethylene glycol poisoning

• Raised LDH with pink coloured plasma inhemolysis

• Anemia with monoclonal spikes in multiple myeloma

• Raised LDH with hyperuricemia and hypocalcemia in tumour lysis syndrome

LABORATORY FINDINGS IN ACUTE RENAL FAILURE:

INDEX PRERENAL

AZOTEMIA

OLIGURIC RENAL FAILURE

BUN/Pcr ratio >20:1 10-15:1

Urine sodiun UNa, meq/L

<20 >20

Urine osmolality mosm/L H2O

>500 <350

Fractional excretion of sodium

<1% >2%

Urine /plasma creatnine Ucr/Pcr

>40% <20%

Urinalysis (casts) None or hyaline granular Muddy brown

FENa= U Na×Pcr×100 PNa×U cr

BUN-blood urea nitrogen

Pcr– Plasma creatinine concentration

PNa– Plasma sodium concentration

Ucr- Urine creatinnine concentration

UNa- Urine sodium concentration

URINARY INDICES:

PRERENAL AKI:

• Specific gravity>1.018

• Urine sodium<10 mmol/litre

• Urine creatinine/plasma creatinine>40

• Urine urea nitrogen/plasma urea nitrogen>8

• Renal failure index<1

• Hyaline casts

• FeNA <1%

• Urine osmolality>500

INTRINSIC AKI:

• Acute glomerulonephritis-FeNA<1%

• Urine sodium <20 mmol/litre

• RBC casts/dysmorphic RBC s

• Acute interstitial nephritis- FeNA >1%

• Eosinophiluria/haematuria

• WBC casts

• DYSMORPHIC RBC

Acute tubular necrosis:

Specific gravity-1.010

FENA>3%

Fractional excretion of urea<60%

Urine sodium>40 mmol/litre

Muddy brown/tubular epithelial casts

It is essential to differentiate between AKI and CKD-presence of following features favours CKD:

 Sustained elevation of creatinine >2 months

 Prior history of renal disease

 Raised parathormone (PTH), serum phosphorus, decrease in serum calcium

 Tolerance to azotemia, acidosis

 Renal bone disease

 Small contracted kidneys with altered renal echoes and loss of corticomedullary differentiation on USG

 Anemia

 Presence of stable azotemia

IMAGING IN AKI:

Ultrasonography: kidney size, echoes, corticomedullary differentiation, renal mass, retroperitoneal mass, hydronephrosis and calculi.

Renal biopsy:

Indications:

1. When etiology of AKI is unknown, prerenal AKI, postrenal AKI, ephrtoxic AKI

2. Interstitial disease , myeloma kidney, HUS, TTP without a definite etiology and allograft rejection

3. Prolonged AKI

4. Systemic disease with AKI-SLE, wegeners granulomatosis

Complications of kidney biopsy- bleeding, thrombocytopenia and coagulopathy.

Radionucleotide scan: for assessing blood flow.

Intravenous urography : to assess hydronephrosis, kidney size and function, hydroureter, bladder outlet obstruction, bladder size.

MARKERS OF KIDNEY FUNCTION:

No single marker can predict kidney function.

UREA CLEARANCE:

Urea elimination is a complex process. non renal etiologies for urea elimination are total parentral nutrition, steroid use, gastrointestinal bleeding.

Factors other than GFR can implicate plasma urea levels, so urea is considered as less useful marker for assessing renal function.

CREATININE:

Routinely used for calculating GFR.

Metabolic product of creatine is creatinine. Proximal tubular secretion(10%) with Glomerular filtration (90%) eliminates creatinine.

With detoriation in renal function , tubular secretion raises upto 50%.

Glomerular filtration rate(GFR):

GFR is the sum of filtration rate of nephrons (functional).

Normal GFR IS 125 ml/min/1.73 m²in males

100 ml/min/1.73 m² in females

GFR=U*V/P

Where p- concentration of substance in plasma

U concentration of substance in urine

V urine flow rate

Inulin was previously used as marker of GFR, not used now due to certain limitations,

The substrate used for assessing GFR should be neither secreted nor absorbed by the tubules, should not undergo degradation by the kidney, biologically inert, completely and freely filtered by the glomerulus.

ESTIMATION OF GFR AND CREATININE CLEARANCE:

COCKCROFT GAULT FORMULA

Estimated creatinine clearance: = (140-age)×body weight×0.85 (if female) 72×plasma creatinine

MDRD EQUATION :

Est. GFR = 170 × (PCr)^-0.999× (age)^-0.175× (0.762 if female) × (1.180 if African American) × (BUN)^-0.170× (albumin)^+0.318.

Both these equations overestimate the GFR in severe renal dysfunction and underestimate GFR in normal kidney function.

PITFALLS OF CREATININE AS A MARKER OF AKI:

 Varies with muscle mass (creatinine spuriously high in muscular patient and low in wasted patient)

 Drugs like cimentidine, trimethoprim interferes with creatinine secretion Production of creatine deponds on certain factors like race, age, body mass Based on a baseline creatine value, changes in creatinine should be interpreted Creatinine acts as a useful marker of GFR in steady state only.

 Current eGFR equations are used to estimate kidney function when plasma creatinine is stable but they are not appropriate if the plasma creatinine is changing rapidly. When the serum creatinine is changing, GFR cannot be reliably estimated by any of the steady state formulas that use a single creatinine input. Instead GFR needs to be estimated by a more general equation that takes into account creatinine kinetics. i.e., how fast the serum creatinine is changing usingkinetic gfr (KeGFR)

To overcome this, in our studykinetic GFR(KeGFR)formula is used to assess the renal function(for calculating GFR)

KINETIC GFR (KeGFR):

The formula is derived from initial creatinine content, creatinine production rate, volume of distribution and the difference between the consecutive plasma creatinine over time.

/ min = ∗

∗ [1 − 24 ∗ ( − )

( − ) ∗ 1.5]

Variable Definition Baseline creatinine, mg/dl

Initial creatinine, ML/min (by MDRD equation)

Average of Cr1-Cr2

− Time between measured Cr2 and Cr1 , hrs

MANAGEMENT OF AKI:

PREVENTION:

No specific treatment modalities available for ischemic and nephrotoxic AKI. Paramount importance is prevention. Specific attention to cardiovascular function and intravascular volume in high risk patients like elderly and with preexisting renal diseases can prevent ischemic AKI.

Ischemic AKI due to trauma, major surgery, burns, aggressive restoration of intravascular volume decreases the incidence of AKI. By altering the dose and frequency of nephrotoxic drugs, incidence of nephrotoxic AKI can be prevented. Drug dosage adjustment according to the bioavailability of drugs appear to decline the kidney injury.

Drugs used are NSAIDS, ACE inhibitors, Angiotensin receptor blockers should be used cautiously in suspected case of renovasular disease and hypovolemia. For acute urate nephropathy, allopurinol and forced alkaline diuresis are used as prophylactic therapy and reduces the precipitation of uric acid crystals in renal tubules.

Hydration is the effective preventive approach for radiocontrast induced nephropathy. Volume expansion with bicarbonate containing IV fluid is superior to normal saline administration. Acetaminophen induced kidney injury is limited by the use of N acetyl cysteine which is given within 24 hours of ingestion.

SPECIFIC TREATMENT:

Prerenal AKI is reversible on correction of hemodynamic abnormality. Post renal KI resolves on relief of obstruction.

PRERENAL AKI:

Isotonic saline can be used in case of moderate plasma loss or hemorrhage (burns or pancreatitis). Severe hypovolemia due to hemorrhage is treated with packed red blood cells.

Inotropic agents are used, preload and afterload reducing agents and intraaortic balloon pump are used are used for cardiac failure. In urinary and gastrointestinal loss, hypotonic fluid is used. Serum potassium and acid base should be monitored carefully and potassium with bicarbonate supplementation is given. Fluid management is difficult in cirrhosis patients. Reversible AKI due to true or effective hypovolemia must be distinguished from hepatorenal syndrome (HRS).

Fluid is administered slowly based on JVP, CVP and PCWP. Transjugular intrahepatic portosystemic stent shunting improve renal function in refractory ascites by increasing central volume and suppression of aldosterone and noradrenaline secretion.

INTRINSIC AKI:

To hasten the recovery and to attenuate the injury in nephrotoxic and ischemic AKI, loop diuretic, low dose dopamine, endothelial antagonists, calcium channel blockers, prostaglandin analogues, antibodies against leucocyte adhesion molecules, antioxidants, and IGF type 1.

AKI due to vasculitis and glomerulonephritis are treated with steroids and immunosupressants. For malignant hypertension, aggressive control of BP is essential.

POSTRENAL AKI:

Obstruction to bladder neck and urethra is initially managed by transurethral or suprapubic bladder. Ureteric obstruction is managed by percutaneous catherisation of dilated renal pelvis or ureter.

PERITONEAL DIALYSIS

In peritoneal dialysis, 1.5–3 L of a dextrose-containing solution is infused into the peritoneal cavity and allowed to dwell for a set period of time, usually 2–4 h. the toxic materials in the body are removed through a combination of two mechanisms :

1. Convective clearance – Movement of solutes out of blood compartment along with movement of water or ultrafiltration . Irrespective of the molecular size, solutes are dragged along with water (solvent drag)

2. Diffusive clearance- solute transport from a region of higher concentration to a region of lower concentration through a semipermeable membrane.

The clearance of solutes and water during a peritoneal dialysis

into the peritoneal cavity versus absorption from the peritoneal cavity. The rate of diffusion diminishes with time and eventually stops when equilibration between plasma and dialysate is reached. Absorption of solutes and water from the peritoneal cavity occurs across the peritoneal membrane into the peritoneal capillary circulation and via peritoneal lymphatics into the lymphatic circulation. The rate of peritoneal solute transport varies from patient to patient and may be altered by the presence of infection (peritonitis), drugs, and physical factors such as position and exercise.

Forms of PD:

1. CAPD – Continuous ambulatory peritoneal dialysis.

2. CCPD – Continuous cyclical peritoneal dialysis

In CAPD, dialysate is manually infused into the peritoneal cavity and exchanged three to five times during the day. A night time dwell is frequently instilled at bedtime and remains in the peritoneal cavity through the night.

In CCPD, exchanges are performed in an automated fashion, usually at night; the patient is connected to an automated cycler that performs a series of exchange cycles while the patient sleeps. The number of exchange cycles required to optimize peritoneal solute clearance varies by the peritoneal membrane characteristic.

HEMODIALYSIS:

Hemodialysis is by far the most commonly used form of renal replacement therapy. The toxic materials are removed through convective and diffusive clearance like PD

Intermittent hemodialysis (IHD) typically runs for 3 to 4 hours per session and is performed three times weekly.

Continuous renal replacement therapy (CRRT) can be used when the patient’s hemodynamic status would not tolerate the rapid fluid shifts of IHD.

Although less efficient (with slower blood flows) and utilizing slower UF rates, CRRT can achieve equivalent clearances of both solute and fluid as compared to IHD due to its continuous, 24-hour nature. The slower blood flows necessitate anticoagulation (with systemic heparin or regional citrate) in order to prevent the filter from clotting. Continuous modalities generally require specialized nursing and an intensive care setting.

The most frequently employed form of CRRT is continuous veno-venous hemodiafiltration (CVVHDF).

In CVVHDF, blood is slowly pumped counter-currently to a dialysis solution (diffusion) and a replacement fluid (a “cleansed” physiologic solution devoid of uremic toxins) is infused into the circuit to balance most of the ultrafiltration (convection).

PRESCRIPTION AND ADEQUACY:

Sustained low efficiency dialysis (SLED) is essentially a hybrid form of IHD and CRRT used in an intensive care setting. Intermediate blood flows lower the clotting risk if anticoagulation is not used, while intermediate treatment lengths (8 to 10 hours) still allow for adequate clearances. Patients also spend a significant portion of the day off the machine to allow for non bedside testing, procedures, and physical therapy.

IHD typically runs for 3 to 4 hours and can ultrafiltrate 3 to 4 L safely in hemodynamically stable patients. It can be used in ESRD as well as AKI. In the chronic setting, IHD is generally performed three times weekly. In the acute setting, the appropriate interval is not clearly known, although a thrice-weekly schedule is likely adequate daily assessment should be performed to reevaluate dialytic needs.

Adequacy is assessed by calculating the clearance of BUN, which serves as a surrogate marker of the “uremic factors.” The urea reduction ratio (URR) can be calculated by the following:

URR = [(predialysis BUN–postdialysis BUN)/(predialysis BUN)] *100 A reduction rate of >65% is considered adequate in the chronic setting PROGNOSIS OF AKI:

Acute kidney injury (AKI) is common (especially during critical illness), increasing in incidence, and is associated with considerable morbidity

(RIFLE) classification currently provides a standardized estimate of incidence and outcomes from AKI. Despite advances in the understanding of the pathogenesis of human AKI, our ability to assess kidney function is limited and functional impairment poorly correlates with structural injury to the kidneys.

Emerging novel biomarkers are, however, likely to further enhance risk stratification, facilitate early diagnosis, enable early enrollment in therapeutic trials, and assess prognosis. Sepsis remains the leading cause of AKI among the critically ill and over the past few years insights into the pathogenesis of AKI in sepsis are beginning to shift attention from renal blood flow to inflammation-mediated organ injury. Emerging evidence suggests that survivors of AKI incur long-term risks for developing chronic kidney disease and end-stage renal disease compared with those without AKI. Despite decades of research, no specific therapy for AKI other than supportive care currently exists and further work is required to better understand the pathogenesis of AKI during critical illness and to develop novel treatments.

OUTCOME OF AKI:

• AKI is associated with in hospital mortality and increased duration of hospital stay and increased cost of treatment.

• Post renal AKI and Prerenal AKI with exception of hepatorenal and cardiorenal syndromes carries better prognosis.

• Even after severe AKI requiring dialysis, kidneys recover. AKI survivors who had temporary dialysis requirement can progress to CKD ((end stage renal disease).

• Aggressive secondary prevention measures with post discharge care is mandatory.

NOVEL BIOMARKERS OF AKI:

BUN and creatinine are functional biomarkers of GFR and used fot the diagnosis of acute parenchymal kidney disease.

KIDNEY INJURY MOLECULE (KIM):

Type 1 transmembrane protein that is abundantly expressed in proximal tubular cells injured by ischemia/nephrotoxin. It confers phagocytic properties to tubular cells, clears debris from the tubular cells and reduce the inflammatory response to acute kidney.

It is detected shortly after ischemic/ nephrotoxic injury and considered as easily tested biomarker in the clinical setting.

NEUTROPHIL GELATINASE ASSOCIATED LIPOCALCIN (NGAL/LIPOCALCIN/SIDEROCALCIN):

Another novel biomarker.

Highly upregulated after inflammation and kidney injury. NGAL can bind to iron siderophore complexes and have tissue protective effects in the renal tubules.

URINE CYSTATIN –C:

Poor predictor of AKI. Reabsorbed through megalin receptor in proximal tubules.Dueto increased urine albumin in sepsis, sepsis per se will increase urine cystatin levels through competitive inhibion of megalin receptors.

INTERLEUKIN -18:

Varying ability to predict AKI.

It is a pro inflammatory cytokine secreted by proximal tubular cells and leucocytes.

N-ACETYL –d-GLUCOSAMINIDASE (NAG):

Lysosomal enzyme found in several human cells including tubular epithelial cells , >130 dalton not filtered, elevated levels in severe acute renal diseases.

URINARY LIVER TYPE FATTY ACID BINDING PROTEIN (L-FABP):

Is a fatty acid binding protein , with molecular weight of approximately 14 dalton, confined to proximal tubular epithelial cells. Normally it is found in the cytotoplasm of proximal tubular epithelial cells and rapidly released into the tubular lumen in response to ischemia and oxidative stress.

 ALKALINE PHOSPHATASE

 ALANINE AMINOPEPTIDASE

 BETA 2 MICROGLOBULIN

 ALPHA GLUTHATIONE –S- TRANSFERASE

 RETINOL BINDING PROTEIN

 ALPHA 1 MICROGLOBULIN

 MICROALBUMIN

 OSTEOPONTIN

 CLUSTERIN

 HAPTOGLOBIN, HEME OXYGENASE

 FIBULIN-1

 INSULIN LIKE GROWTH FACTOR BINDING PROTEIN -7(IGFBP7)

 TISSUE INHIBITOR OF METTALOPROTEINASE-2(TIMP-2)

 L-FABP, URINE IL -18-proposed biomarkers

MATERIALS AND METHODS

Sample size-100

Type of study-Prospective study

Duration of study-One year

Area of Study –Tirunelveli Medical College (Tertiary Care Hospital)

Statistical analysis:

Statistical analysis was performed using SPSS VERSION 21 software. .All categorical data are expressed as percentage. The continous variables are expressed as Mean ±Standard deviation. Statistical analysis are performed using anova test, unpaired test and kruskal wallis test. Variables with p values <0.05 is considered significant.

Study design and sampling

100 patients admitted with AKI are defined according to AKI Network criteria (AKIN) among 1500 acute care hospital admissions in Tirunelveli medical college. Their clinical and biochemical data were studied. The patients were followed up until discharge/death.

INCLUSION CRITERIA:

2.Patients with increase in serum creatinine of 0.3 mg/dl from the baseline or elevation of >50% from the baseline (based on AKIN criteria), reduced glomerular filtration rate (GFR) and urine output < 0.3ml/kg/hr for 24 hours or anuria for12 hours (based on failure category of RIFLE criteria of acute kidney injury).

EXCLUSION CRITERIA:

1.Pregnancy

2. Age less than 12 years

3. Chronic contracted kidneys

METHODOLOGY:

Patients fullfilling the inclusion and exclusion criteria were included in this study conducted from February 2018 to February 2019 .

Written informed consent was obtained from the patients selected for the study. Ethical committee approval obtained. History collected from the patient and subjected to clinical examination, routine blood investigations including blood urea, serum creatinine, urine routine, ultrasound abdomen, serology for leptospirosis, enteric fever, peripheral smear for malarial parasite and other relevant investigations were performed and values interpreted. Patients were started on appropriate therapy once a diagnosis was made. Wherever possible

etiological factors were corrected. Renal replacement therapy was given according to their clinical and biochemical indications.

Patients with raise in serum creatinine 0.3 mg/dl from the baseline or> 50%

elevation from the baseline were followed up and studied.

RESULTS

AGE DISTRIBUTION

AGE IN YEARS NO OF PATIENTS PERCENTAGE

< 20 9 9%

21-30 14 14%

31-40 14 14%

41-50 21 21%

51-60 26 26%

> 60 16 16%

9%

14%

14%

21%

26%

16%

AGE DISTRIBUTION

< 20 21-30 31-40 41-50 51-60 > 60

SEX DISTRIBUTION

SEX NO OF PATIENTS PERCENTAGE

MALE 63 63%

FEMALE 37 37%

63%

37%

SEX DISTRIBUTION

MALE FEMALE

SYMPTOMS

SYMPTOMS PRESENT ABSENT

OLIGURIA 66 34

FEVER 36 64

VOMITTING 5 95

LOOSE STOOLS 22 78

PEDAL EDEMA 11 89

JAUNDICE 3 97

66

36

5 22

11 3

34

64

95 78

89 97

OLIGURIA FEVER VOMITTING LOOSE

STOOLS PEDAL

EDEMA JAUNDICE

SYMPTOMS

PRESENT ABSENT

CAUSES

CAUSES PRESENT ABSENT

SEPSIS 22 78

HYPOTENSION 16 84

AGE 19 81

SNAKE BITE 15 85

POISONING 6 94

GLOMERULONEPHRITIS 7 93

FEVER 6 94

DRUGS 1 99

BOO 3 97

RENAL CALCULI 5 95

INJURY 2 98

BURNS 2 98

PANCREATITIS 1 99

22 16

19 15 6

7 6 1

3 5 2 2 1

78 84

81 85 94

93 94 99

97 95 98 98 99

SEPSIS HYPOTENSION AGE SNAKE BITE POISONING GLOMERULONEPHRITIS FEVER DRUGS BOO RENAL CALCULI INJURY BURNS PANCREATITIS

CAUSES

PRESENT ABSENT

LEUCOCYTOSIS

LEUCOCYTOSIS NO OF PATIENTS PERCENTAGE

PRESENT 19 19%

ABSENT 81 81%

19%

81%

LEUCOCYTOSIS

PRESENT ABSENT

THROMBOCYTOPENIA

THROMBOCYTOPENIA NO OF PATIENTS PERCENTAGE

PRESENT 14 14%

ABSENT 86 86%

14%

86%

THROMBOCYTOPENIA

PRESENT ABSENT

HYPERKALEMIA

HYPERKALEMIA NO OF PATIENTS PERCENTAGE

PRESENT 6 6%

ABSENT 94 94%

6%

94%

HYPERKALEMIA

PRESENT ABSENT

URINE SODIUM

URINE SODIUM NO OF PATIENTS PERCENTAGE

< 20 31 31%

> 20 69 69%

31%

69%

URINE SODIUM

< 20 > 20

KINETIC GFR

KINETIC GFR NO OF PATIENTS PERCENTAGE

LESS THAN 10 62 62%

10 TO 20 19 19%

20 TO 30 19 19%

19% 62%

19%

KINETIC GFR

LESS THAN 10 10 TO 20 20 TO 30

PROTEINURIA

PROTEINURIA NO OF PATIENTS PERCENTAGE

PRESENT 7 7%

ABSENT 93 93%

7%

93%

PROTEINURIA

PRESENT ABSENT

TYPE OF AKI

TYPE OF AKI NO OF PATIENTS PERCENTAGE

PRE RENAL 29 29%

RENAL 63 63%

POST RENAL 8 8

29%

63%

8%

TYPE OF AKI

PRE RENAL RENAL POST RENAL

CONSERVATIVE TREATMENT

CONSERVATIVE TRT NO OF PATIENTS PERCENTAGE

DONE 62 62%

NOT DONE 38 38%

62

38

DONE NOT DONE

CONSERVATIVE

HEMODIALYSIS

HEMODIALYSIS NO OF PATIENTS PERCENTAGE

DONE 24 24%

NOT DONE 76 76%

DONE NOT DONE

24

76

HEMODIALYSIS

PERITONEAL DIALYSIS

PERITONEAL DIALYSIS NO OF PATIENTS PERCENTAGE

DONE 14 14%

NOT DONE 86 86%

DONE NOT DONE

14

86

PERITONEAL DIALYSIS

TREATMENT

TREATMENT NO OF PATIENTS PERCENTAGE

CONSERVATIVE 62 62%

HEMODIALYSIS 24 24%

PERITONEAL DIALYSIS 14 14%

62%

24%

14%

TREATMENT

CONSERVATIVE HEMODIALYSIS PERITONEAL DIALYSIS

GENERAL PARAMETERS

IN ALL PATIENTS

PARAMETERS MEAN SD

AGE 44.22 15.91

BLOOD UREA 116.39 46.24

BASELINE CREATININE 1.02 0.19

CREATININE 2 2.06 0.67

CREATININE AT DIAGNOSIS 3.22 1.39

SODIUM 137.98 7.46

POTASSIUM 4.5 0.86

URINE SODIUM 31.06 12.96

OUTCOME

OUTCOME NO OF PATIENTS PERCENTAGE

FULL RECOVERY 77 77%

PARTIAL RECOVERY 15 15%

DEATH 8 8%

77%

15%

8%

OUTCOME

FULL RECOVERY PARTIAL RECOVERY DEATH

OUTCOME VS UREA LEVEL

OUTCOME BLOOD UREA

MEAN SD

FULL RECOVERY 117.58 48.42

PARTIAL RECOVERY 106.36 36.35

DEATH 123.62 43.12

ANOVA P VALUE - 0.627 NON SIGNIFICANT

117.58

106.36

123.62

FULL RECOVERY PARTIAL RECOVERY DEATH

OUTCOME VS UREA LEVEL

OUTCOME VS CREATININE AT DIAGNOSIS

OUTCOME CREATININE ON DIAGNOSIS

MEAN SD

FULL RECOVERY 3.33 1.48

PARTIAL RECOVERY 2.7 0.86

DEATH 3.16 1.16

ANOVA P VALUE - 0.279 NON SIGNIFICANT

FULL RECOVERY PARTIAL RECOVERY DEATH 3.33

2.7

3.16

OUTCOME VS CREATININE LEVEL

CONSERVATIVE TRT VS UREA LEVELS

CONSERVATIVE BLOOD UREA

MEAN SD

DONE 108.18 42.33

NOT DONE 129.31 49.67

UNPAIRED T TEST P VALUE - 0.001 NON SIGNIFICANT

DONE NOT DONE

108.18

129.31

CONSERVATIVE VS BLOOD UREA

CONSERVATIVE TRT VS CREATININE ON DIAGNOSIS

CONSERVATIVE CREATNINE ON DIAGNOSIS

MEAN SD

DONE 2.63 1.11

NOT DONE 4.14 1.3

UNPAIRED T TEST P VALUE - 0.001 NON SIGNIFICANT

2.63

4.14

DONE NOT DONE

CONSERVATIVE VS CREATININE

HEMODIALYSIS VS BLOOD UREA

HEMODIALYSIS BLOOD UREA

MEAN SD

DONE 114.75 43.27

NOT DONE 117.7 46.23

UNPAIRED T TEST P VALUE - 0.976 NON SIGNIFICANT

114.75

117.7

DONE NOT DONE

HEMODIALYSIS VS BLOOD UREA

HEMODIALYSIS VS CREATININE AT DIAGNOSIS

HEMODIALYSIS CREATININE ON DIAGNOSIS

MEAN SD

DONE 3.7 1.65

NOT DONE 3.07 1.46

UNPAIRED T TEST P VALUE - 0.05

SIGNIFICANT

DONE NOT DONE

3.7

3.07

HEMODIALYSIS VS CREATININE

PERITONEAL DIALYSIS VS BLOOD UREA

PERITONEAL DIALYSIS BLOOD UREA

MEAN SD

DONE 154.71 47.13

NOT DONE 110.15 43.24

UNPAIRED T TEST P VALUE - 0.001

SIGNIFICANT

154.71 110.15

DONE NOT DONE

PERITONEAL DIALYSIS VS BLOOD

UREA

PERITONEAL DIALYSIS VS CREATININE AT DIAGNOSIS

PERITONEAL DIALYSIS CREATININE ON DIAGNOSIS

MEAN SD

DONE 5.1 1.13

NOT DONE 2.91 1.18

UNPAIRED T TEST P VALUE - 0.001

SIGNIFICANT

DONE NOT DONE

5.1 2.91

PERITONEAL DIALYSIS VS CREATININE

TREATMENT VS BLOOD UREA

TREATMENT BLOOD UREA

MEAN SD

CONSERVATIVE 108.18 42.33

HEMODIALYSIS 114.45 43.27

PERITONEAL DIALYSIS 154.71 47.13

ANOVA P VALUE - 0.003

SIGNIFICANT

CONSERVATIVE HEMODIALYSIS PERITONEAL DIALYSIS

108.18 114.45

154.71

TREATMENT VS MEAN UREA

TREATMENT VS CREAININE AT DIAGNOSIS

TREATMENT SERUM CREATININE @ DIAGNOSIS

MEAN SD

CONSERVATIVE 2.63 1.11

HEMODIALYSIS 3.7 1.65

PERITONEAL DIALYSIS 5.1 1.13

ANOVA P VALUE - 0.003

SIGNIFICANT

2.63

3.7

5.1

CONSERVATIVE HEMODIALYSIS PERITONEAL DIALYSIS

TREATMENT VS CREATININE LEVELS

OUTCOME VS CONSERVATIVE TREATMENT

OUTCOME CONSERVATIVE TREATMENT

DONE NOT DONE

FULL RECOVERY 46 31

PARTIAL RECOVERY 10 5

DEATH 6 2

KRUSKAL WALLIS TEST P VALUE - 0.877 NON SIGNIFICANT

46

31

10 6 5

2

DONE NOT DONE

CONSERVATIVE TREATMENT

CONSERVATIVE TRT VS OUTCOME

FULL RECOVERY PARTIAL RECOVERY DEATH