ACUTE RENAL FAILTURE LIJI VINCENT

Acute renal failure (ARF) refers to a sudden and usually reversible loss of renal function, which develops over a period of days or weeks and is usually accompanied by a reduction in urine volume.

Reversible Pre-Renal Acute Renal Failure Pathogenesis

Clinical Features Hypotension and signs of poor peripheral perfusion Postural hypotension fall in SBP/DBP >20/10 mmHg early sign of hypovolaemia. The cause of reduced renal perfusion may be obvious or concealed Metabolic acidosis and hyperkalaemia may be (+)

Management Establish and correct the underlying cause of the ARF. If hypovolaemia (+) replace with blood, plasma or isotonic saline Optimise systemic haemodynamics. Monitor CPU or pulmonary a wedge pressure. Correct metabolic acidosis - Restoration of blood volume will restore kidney function - Isotonic sodium bicarbonate

Established Acute Renal Failure Following severe or prolonged under perfusion of the kidney. Histology: Acute tubular necrosis Acute Tubular Necrosis: Cause (1) Ischaemia (2) Nephrotoxicity

Direct toxicity of the causative agent to the tubular cells. Nephrotoxic ATN Direct toxicity of the causative agent to the tubular cells.

Recovery From ATN Tubular cells can regenerate If the patient is supported during the regeneration phase. Kidney function restores Recovery phase-Diuretic phase

Other feature Uraemic features- anorexia, nausea and vomiting drowsiness, apathy, confusion, muscle twitching Respiratory rate increased – Acidosis, pulmonary oedema, infection. Anaemia – Blood loss, haemolysis disordered platelet function and disturbances of the coagulation cascade.

Clinical Features of Established ARF Reflect the causal condition – trauma, septicemia or systemic diseases + 1. Alterations in urine volume Oliguric (<500ml/daily) Anuria Non Oliguric - Normal or Increased Disturbances of water, electrolyte and acid – base balance Hyperkalaemia - massive tissue breakdown, haemolysis Dilutional hyponatraemia.

URINARY TRACT OBSTRUCTION SUGGESTED BY LOIN PAIN, RENAL COLIC OR DIFFICULTY IN MICTURITION INVES- USG PROMPT RELIEF OF OBSTRUCTION RESTORES KIDNEY FUNCTION

VASCULAR EVENT MAJOR VASCULAR OCCLUTION OR SMALL VESSEL DISEASE URINE SHOW MINIMAL ABNORMALITIES MAY BE PRECIPITATED BY ACE INHIBITORS

RPGN SIGNIFICANT DIP STICK HAEMATURIA ASSOSIATED WITH SYSTEMIC FEATURES BLOOD TESTS-ANA, ANCA, ANTI-GBM ANTIBODIES DIAGNOSIS- RENAL BIOPSY

ACUTE INTERSTITIAL NEPHRITIS CAUSED BY ADVERSE DRUG REACTION SMALL AMOUNT OF BLOOD AND PROTIEN IN URINE KIDNEYS NORMAL IN SIZE Tt-CESSATION OF DRUG AND PREDNISOLONE

DRUGS HAEMODYNAMIC EFFECTS- NSAIDs , ACE INHIBITORS DIRECT TOXICITY TO THE TUBULES- AMINOGLYCOSIDES

Screening Tests Hematology Full blood count Blood film Clotting screen, Group and save Biochemistry Urea, electrolytes and creatinine calcium Urinalysis Urine Microcopy Quantitative urinary protein measurement

3. Microbiology Blood culture CRP Mid-stream urine Other cultures 4. Imaging Renal USG Chest X ray ECG

Immunoglobulin and protein electrophoresis Urinary Bence Jones Protein Complement ANA and ds DNA Extractable nuclear Antigen (ENA) Rheumatoid factor

Management 1.Emergency resuscitation Hyperkalaemia – treated immediately Circulating blood volume restoration Acidosis-Isotonic sodium bicarbonate 2.Addressing the underlying cause USG showing urnary tract obstruction. ATN - restoring renal perfusion. Postrenal obstruction :Due to Pelvic or ureteric dilatation – Percutaneous nephrostomy

Fluid and electrolyte balance Daily fluid intake should = prev. day urine output + 500ml to cover unsensible loss. Abnormal loses like diarrhea – electrolyte replacement. Since Na+ and K+ are retained their intake should be restricted Protein and energy intake In patients where dialysis is avoided – protein restriction to 40g/day In patients with dialysis – more dietary protein

Infection control Regular clinical examination and microbiological investigation required. Drugs Vasoactive drugs NSAIDs & ACE inhibitors are to be avoided. Renal Replacement therapy This may be required as supportive management in ARF.

Increased Plasma urea andcreatinine urea >30mmol/l Creatinine >6.8mgdl At lower level – Progressive biochemical deterioration. Hyperkalaemia – K+ >6mmol Metabolic acidosis raise the plasma potassium further. Fluid overload and pulmonary oedema Uraemic pericarditis/ uraemic encephalopathy.

Intermittent haemodialysis Best rate of small solute clearance.1 hour tt is prescribed. Subsequently when haemodyamically stable 3 – 4 hours 3 – 4 times a week. Haemodialysis 2 – 3 hrs every day – severly catabolic

Haemofiltration Intermittent 15 – 30 liters of plasma ultra filtrate exchanged for replacement fluid over 3 – 5 hours. Continuous 1 – 2 liters of filtrate replaced higher rate of filtration MODS sepsis.

Intermittent haemodiafiltration

Peritoneal dialysis Seldom achieves adequate biochemical control

Difference BetweenHD&PD Efficient Less efficent 4hours 3 times a week 4 exchanges per day each 30 60 min. – CAPD or 8 -10 hrs Automated PD 2-3 day between Few hrs between tt Requires visit to hospital Performed at home Requires adequate venous acces Requires an intact peritoneal cavity

Careful compliance to diet and fluid restriction Diet & fluid less restricted Fluid removal compressed during tt period - haemody instability Slow continous fluid removal - asymptomatic Infection reld to vascular access Infection – Peritonitis,catheter reld infections Patients are, to some extent dependent on others Patients can take full reponsibility of their tt