4.Acute renal failure.Dr.Thilak Jayalath_Renal Lectures
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4.Acute renal failure.Dr.Thilak Jayalath_Renal Lectures






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4.Acute renal failure.Dr.Thilak Jayalath_Renal Lectures 4.Acute renal failure.Dr.Thilak Jayalath_Renal Lectures Document Transcript

  • 1 Acute renal failure ARF is defined as a reduction in glomerular filtration rate (GFR) occurring over days or weeks ((In routine clinical practice, measurement of serum creatinine is used to follow changes in GFR) This is due to abrupt deterioration in parenchymal renal function, which is usually, but not invariably, reversible over a period of days or weeks Acute renal failure may cause sudden, life-threatening biochemical disturbances and is a medical emergency Common causes of ARF in Sri Lanka Leptospirosis Viper bites Acute glomerulonephritis Septicemia Common working definitions of ARF An increase in serum creatinine of > 50 µmol/litre An increase in serum creatinine of > 50% from baseline A reduction in calculated creatinine clearance of > 50% Need for dialysis Considerable caution is required in interpreting measurements of serum creatinine in ARF Creatinine production depends on muscle mass, and though normally constant can increase in patients with acute muscle injury (as in rhabdomyolysis) Creatinine concentration may exhibit a modest decrease as a result of dilution during rapid fluid resuscitation (e.g. an increase in extracellular fluid volume from 12 litres to 14 litres reduces serum creatinine from 300 to 257 µmol/litre) Because of the reciprocal relationship between creatinine concentration and GFR, small changes in GFR close to the normal range have much less effect on serum creatinine than small changes when GFR is already significantly reduced Changes in serum creatinine concentration lag behind changes in GFR Creatinine concentration may continue to increase for several days after a sudden marked reduction in GFR, even if GFR starts to improve immediately Dr.Thilak Jayalath MBBS MD FRCP FRCPE FISN Senior Lecturer in Medicine & Consultant Physician Department of Medicine, Peradeniya
  • 2 Clinical Features In the early stages of acute renal failure there are few warning symptoms The patient may notice a reduction in urinary volume, but non-oliguric renal failure is not uncommon Effects of intravascular volume depletion, with dizziness caused by postural hypotension In the later stages of acute renal failure There are manifestations of uraemia with anorexia, nausea, vomiting (or occasionally diarrhoea), muscular cramps, and signs of encephalopathy—including a ‘metabolic’ flapping tremor (asterixis) Skin bruising and gastrointestinal bleeding may occur Uraemic haemorrhagic pericarditis is another potentially fatal complication, but this occurs much less frequently in acute renal failure than in (neglected) chronic renal failure Causes of acute renal failure Pre renal failure Renal failure due to intrinsic renal disease Post renal failure Pre renal failure This is an appropriate physiological response to effective or true hypovolaemia, resulting in intense renal conservation of sodium and water at the expense of decreased GFR The kidneys are normal without cellular injury The elderly at high risk because of their predisposition to hypovolemia and renal atherosclerotic disease Urea clearance decreases more than creatinine clearance as a result of the action of antidiuretic hormone (ADH) Renal function returns to normal rapidly once the underlying cause is corrected. Causes of pre renal failure Severe hypovolemia Severe hypotension Renal failure due to intrinsic renal disease • destruction of glomeruli • renal arteriolar vasoconstriction (e.g. contrast nephropathy) • ischaemic damage, resulting in ATN • direct tubular toxicity, resulting in an ATN-like syndrome impaired cardiac pump efficiency vascular disease limiting renal blood flow
  • 3 Causes of acute renal failure secondary to intrinsic renal disease Acute tubular necrosis Renal parenchymal disease Nephrotoxicity Hepatorenal syndrome Impaired renal perfusion + drug-induced impairment of autoregulation Rhabdomyolysis Contrast nephropathy Urate nephropathy Renal vein thrombosis Myeloma 1. Acute tubular necrosis This results from the insults that cause pre-renal ARF, but lasting long enough to cause ischaemic injury to renal tubules This leads to a long-lasting reduction in GFR that sometimes persists for weeks after correction of the initiating insult This is caused by a combination of • Persistent, intense intra-renal vasoconstriction caused by endothelin, other autocrine mediators and increased intra-cellular calcium • Loss of polarity of tubular cells, leading to loss of function • Loss of adherence of tubular cells, leading to desquamation into the tubular lumen formation of tubular casts, blocking the lumen and preventing urine flow • tubulo-glomerular feedback (reflex reduction of glomerular perfusion caused by high sodium concentration in the distal tubule) • Back-leak of tubular filtrate as a result of loss of tubular viability and obstructing casts • Reperfusion injury, causing oxidant stress. These observations have led to many attempts to alter the natural history of ATN using, for example, vasodilators, natriuretic peptides, diuretics and growth factors, but almost all have been unsuccessful Common causes are • General surgery • Cardiac surgery • Vascular surgery • Obstetric complications • Sepsis • Acute heart failure • Burns
  • 4 2. Renal parenchymal disease • Rapidly progressive glomerulonephritis (systemic vasculitis, Goodpasture’s disease, systemic lupus erythematosus, other forms of glomerulonephritis) • Acute interstitial nephritis • Haemolytic uraemic syndrome • Cryoglobulinaemia 3. Nephrotoxicity aminoglycosides and amphotericin 4. Hepatorenal syndrome Reversible intense renal vasoconstriction and sodium retention complicating cirrhosis 5. Impaired renal perfusion + drug-induced impairment of autoregulation Angiotensin-converting enzyme inhibitors, non-steroidal anti-inflammatory drugs, plus atherosclerotic renal vascular disease or hypovolaemia 6. Rhabdomyolysis Following crush injury, drug overdose, status epilepticus 7. Contrast nephropathy A specific form of nephrotoxicity characterized by renal vasoconstriction and avid sodium retention 8. Urate nephropathy Complicating chemotherapy of acute leukaemia or lymphoma 9. Renal vein thrombosis Complicating malignancy or pre-existing nephrotic syndrome 10. Myeloma Cast nephropathy, light-chain deposition disease, amyloidosis, sepsis and hypercalcaemia can all cause renal damage Post-renal ARF Increased pressure within the renal collecting systems results in Reduced GFR Reduced tubular reabsorption of sodium and water Acquired renal tubular acidosis Phosphaturia Other abnormalities of tubular function Causes of post renal failure Benign or malignant prostatic bladder outflow obstruction Infiltrative bladder cancer (causing bilateral vesico-ureteric obstruction) Other pelvic malignancies Radiation fibrosis
  • 5 Bilateral stone disease Retroperitoneal fibrosis with or without abdominal aortic aneurysm Raised serum creatinine in an acutely unwell patient can be caused by Acute renal failure Acute-on- chronic renal failure Chronic renal failure (CRF) Distinguishing acute from chronic renal failure Renal ultrasonography Determines renal size and echogenicity, and is imperative to exclude hydronephrosis Renal swelling is seen only in ARF Reduced renal volume, length or cortical thickness, together with increased echogenicity, is a feature of many types of CRF, though renal size may remain normal in CRF (e.g. diabetic nephropathy, amyloidosis) Renal size is normal in most patients with ARF Investigations Urine microscopy and urinalysis Red cell casts are highly suggestive of glomerular disease as in rapidly progressive glomerular nephritis WBC casts are suggestine of acute pyelonephritis Broad waxy casts are seen in acute tubular necrosis Haematuria and proteinuria are seen in rapidly progressive glomerular nephritis Urinary electrolytes Measurements of urinary sodium concentration and osmolality are often misleading, particularly in patients who have taken diuretics or dopamine (both of which increase urinary sodium excretion) Very low urinary sodium excretion or fractional excretion of sodium indicates that the ability of the tubules to reabsorb sodium is intact, as in pre-renal ARF, rhabdomyolysis and contrast nephropathy Very high urine osmolality indicates that the tubules are able to reabsorb water under the influence of antidiuretic hormone, and suggests pre-renal ARF Higher urinary sodium levels and lower osmolality are seen in patients with ATN Fractional excretion of urea ([urine urea/plasma urea]/[urine creatinine/plasma creatinine] x 100%) is less affected by diuretic therapy and may be a more useful discriminant of pre-renal ARF and ATN; values of less than 35% suggest pre-renal ARF
  • 6 Distinguishing pre renal failure from intrinsic renal disease Pre renal failure Intrinsic renal disease Urine specific gravity > 1020 < 1010 Urinary Sodium < 20 mmol / L > 30 mmol / L Urinary : plasma osmolality > 1.5 < 1.1 Urine osmolality ( mOsmol / L ) > 500 < 350 Urine to plasma urea ratio > 8 < 3 Urine to plama creatinine ratio > 40 < 20 Fractional sodium excretion < 1 > 1 Fractional urea excretion < 35 % > 35 % Fractional sodium excretion = (urine sodium / plasma sodium) . x 100 (urine creatinine / plasma creatinine) Fractional urea excretion = (urine urea / blood urea) . x 100 (Urine creatinine / plasma creatinine) Blood test abnormalities suggesting specific underlying renal disorders Abnormality Suggested underlying disorder Eosinophilia Acute interstitial nephritis Cholesterol embolism Very high creatine kinase, phosphate, K+ Rhabdomyolysis Elevated lactate dehydrogenase Renal infarction/embolism Antineutrophil cytoplasm antibodies Systemic vasculitis causing rapidly progressive glomerulonephritis Antiglomerular basement membrane antibody Goodpasture’s disease Low C4 complement Systemic lupus erythematosus, cholesterol embolism, cryoglobulinaemia Antinuclear antibody, anti-dsDNA Systemic lupus erythematosus Cryoglobulin Cryoglobulinaemia Plasma urate Urate nephropathy Serum (and urine) electrophoresis Myeloma Renal biopsy Should be considered in all patients with normal-sized, unobstructed kidneys in whom a diagnosis of ATN causing ARF is not suspected Renal biopsy should be performed without delay when there is a clinical suspicion of RPGN (e.g. positive antineutrophil cytoplasm antibodies, haematuria and proteinuria, raised C- reactive protein)
  • 7 Treatment Pre renal failure Rapidly reversible upon correction of the primary haemodynamic abnormality The composition of replacement fluids for treatment of prerenal ARF due to hypovolemia Must be tailored according to the composition of the lost fluid  Severe hypovolemia due to haemorrhage - packed red cells  Mild to moderate haemorrhage or plasma loss - isotonic saline  Mild to moderate loss of urinary & GI losses - hypotonic fluids initially  Severe cases of urinary and GI losses - isotonic saline Post renal failure Management of post renal acute renal failure requires close collaboration between nephrologists, urologist and radiologist Most patients experience an appropriate diuresis for several days following relief of obstruction Approximately 5 % of patients develop a transient salt-wasting syndrome that may require administration of intravenous saline to maintain blood pressure Renal failure due to intrinsic renal disease The clinical course of acute renal failure associated with ATN is variable depending on the severity and duration of the renal insult. Oliguria is common in the early stages: non-oliguric renal failure is usually a result of a less severe renal insult Recovery of renal function typically occurs after 7-21 days, although recovery is delayed by continuing sepsis. In the recovery phase, GFR may remain low while urine output increases, sometimes to many litres a day owing to defective tubular reabsorption of filtrate. The clinical course is variable and ATN may last for up to 6 weeks, even after a relatively short-lived initial insult The aim of management of acute renal tubular necrosis is to keep the patient alive until spontaneous recovery of renal function occurs Poor initial management and late referral result in the arrival in the specialist centre of a patient who is severely uraemic, acidotic and hyperkalaemic, with pulmonary oedema following over enthusiastic intravenous fluid administration and with a Gram-negative septicaemia complicating the presence of an unnecessary indwelling bladder catheter
  • 8 Hypocalcaemia Hyperphosphataemia Sepsis General measures Good nursing and physiotherapy are vital The patient should be confined to bed only if essential Regular oral toilet, chest physiotherapy and consistent documentation of fluid intake and output, and where possible measurement of daily bodyweight to assess fluid balance changes, all have a role Diet With rare exceptions, sodium and potassium restriction are appropriate If it is hoped to avoid dialysis or haemofiltration, protein intake is sometimes restricted to approximately 40 g daily Patients treated by blood purification techniques are more appropriately managed by providing 70 g protein daily or more Hypercatabolic patients will require an even higher nitrogen intake to prevent negative nitrogen balance Fluid and electrolyte balance Twice-daily clinical assessment is needed In general, once the patient is euvolaemic, daily fluid intake should equal urine output plus losses from fistulae and from vomiting, plus an allowance of 500 mL daily for insensible loss Febrile patients will require an additional allowance. Sodium and potassium intake should be minimized If abnormal losses of fluid occur, for example in diarrhoea, additional fluid and electrolytes will be required The development of signs of salt and water overload (peripheral oedema, basal crackles, elevation of jugular venous pressure) or of hypovolaemia should prompt reappraisal of fluid intake Large changes in daily weight reflecting change in fluid balance status should also prompt a reappraisal of the situation Look for following complications and treat Hyperkalaemia Metabolic acidosis Pulmonary oedema Hyponatraemia In refractory cases, dialysis or haemofiltration should be arranged
  • 9 The main indications for blood purification and/or excess fluid removal • Symptoms of uraemia • Complications of uraemia, such as pericarditis • Severe biochemical derangement in the absence of symptoms (especially if a rising trend is observed in an oliguric patient and in hypercatabolic patients) • Hyperkalaemia not controlled by conservative measures • Pulmonary oedema • Severe acidosis • For removal of drugs causing the acute renal failure, e.g. gentamicin, lithium, severe aspirin overdose Practical clinical approach to ARF Immediate Priorities  Recognition & treatment of life- threatening complications  Recognition & treatment of intravascular volume depletion  Diagnosis of the cause of renal failure 1. Recognition & treatment of life- threatening complications  Assess o Airway o Breathing o Circulation  Hyperkalaemia Can cause cardiac arrest without warning Look for ECG changes  ECG appearance in Hyperkalaemia  Tenting of T waves  Increase in PR interval  Widening of QRS complex  Reduction in size of P wave  Disappearance of P wave, further widening of QRS complex  Sinusoidal wave form
  • 10 Treatment IV Calcium 10% Calcium gluconate, 10ml over 60 seconds Should be given immediately & repeatedly until ECG improves IV Insulin & Glucose Rapid acting Insulin 10 IU with 50% glucose 50 ml over 5-10 min Should be given after IV Calcium Haemodialysis or haemofiltration – in refractory cases Cation exchange resins could be used  Pulmonary Oedema  Due to salt and water overload  Patients are restless & confused  Examination reveals sweating Cyanosis Tachycardia Widespread wheez Crepitation in the chest Gallop rhythm Tachypnoea  Investigations reveals Arterial hypoxaemia Widespread interstitial shadowing on chest X-ray Immediate management  Prop up  High concentration O2  Diuretic agents (Frusemide 40-80 mg IV)  IV Morphine (2.5 mg)  Venesection of 500 ml  Haemodialysis or haemofiltration 2. Recognition & treatment of intravenous volume depletion  Ideally CVP line must be inserted Physical signs  Low jugular venous pressure (JVP)  Postural drop in blood pressure Treatment – Correct volume depletion rapidly  Blood  Colloids  Saline
  • 11 3. Diagnosis of the cause of ARF Is the renal failure acute o Small kidney with increase echogenicity o Evedence of renal osteodystrophy Suggest Chronic Renal Disease o Anaemia (normochromic & normocytic) o High carbamylated Hb Is urinary obstruction a possibility? Is glomerulonephritis or vasculitis possible? When blood & proteins found in urine o Exclude  UTI  Vasculitis  Interstitial nephritis