Acute Renal Failure
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ACUTE RENAL FAILURE
Acute renal failure (ARF) is a syndrome
characterized by rapid decline in GFR hours to days, retention of nitrogenous waste products and disturbances in the extra cellular volume, electrolyte and acid base homeostasis.
Is seen as a complication in about 5% of hospital admissions, and up to 30% of intensive care admissions. Oliguria is a common finding but not necessary. ARF is sometimes asymptomatic and is diagnosed by increase in the urea and creatinine.
CLASSIFICATION AND MAJOR CAUSES OF ACUTE RENAL FAILURE (ARF)
I: PRERENAL ARF: A: Hypovolemia 1: Hemorrhage, burns, dehydration 2: GIT fluid loss; vomiting, surgical drainage, diarrhea 3: Renal fluid loss; diuretics, osmotic diuresis (Diabetes mellitus), hypoadrenalism 4: Sequestration in extravascular space; pancreatitis, peritonitis, trauma, burns, severe hypoalbuminemia
B: Low cardiac output: 1: Diseases of myocardium, valves, and pericardium, arrhythmias, tamponade 2: Other: pulmonary hypertension, massive pulmonary embolus, positive pressure mechanical ventilation
C: Altered Renal systemic vascular resistance ratio 1: Systemic vasodilation; Sepsis, antihypertensives, afterload reducers, anesthesia, anaphylaxis 2: Renal vasoconstriction: Hypercalcemia, norepinephrine, epinephrine, cyclosporine, FK 506, amphoterecin B 3: Cirrhosis with ascites (hepatorenal syndrome)
D: Renal hypoperfusion: with impairement of renal autoregulatory responses 1: Cyclooxygenase inhibitors, ACE inhibitors E: Hyperviscosity syndrome 1: Multiple myeloma, macroglobenemia, polycythemia
II: INTRINSIC RENAL ARF 1: Reno-vascular obstruction (Bilateral or unilateral in the setting of one functioning kidney) A: Renal artery obstruction: Atherosclerotic plaque, thrombosis, embolism, dissecting aneurysms, vasculitis B: Renal vein obstruction: Thrombosis, compression
2: Diseases of the glomeruli or renal
microvasculature
A: Glomerulo nephritis and vasculitis B: Hemolytic uremic syndrome: Thrombotic thrombocytopenic purpura, DIC, toxemia of pregnancy, accelerated hypertension, radiation nephritis, SLE, scleroderma
3: Acute tubular necrosis: A: Ischemia: As per pre-renal ARF, Obstetric complications (abruption placenta, post partum hemorrhage) B: Toxins: 1: Exogenous: radio contrast, cyclosporine, antibiotics (aminoglycosides), chemotherapy (cisplatin), organic solvents (Ethylene glycol), acetaminophen, illegal abortificients 2: Endogenous: Rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (myeloma)
4: Interstitial nephritis
A: Allergic; Antibiotics (beta lactums, sulfonamides, trimethoprim, rifampicin), NSAID, diuretics, captopril B: Bacterial; (acute pyelonephritis, leptospirosis), viral (cytomegalovirus), fungal (candidiasis) C: Infiltration: Lymphoma, leukemia, sarcoidosis. D: Idiopathic: 5: Intratubular deposition and obstruction Myeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulphonamides 6: Renal allograft rejection
III: POST RENAL ARF (OBSTRUCTION)
1: Ureteric: Calculi, blood clot, sloughed papillae, cancer, external compression (retroperitoneal fibrosis) 2: Bladder neck ; Neurogenic bladder, Prostatic hypertrophy, calculi, cancer, blood clot 3: Urethra: stricture, Congenital valve, phimosis
Clinical features and differential diagnosis 1: Determine whether decline in GFR it is acute or chronic. Findings that suggest of chronic renal failure are anemia, neuropathy, and radiologic evidence of osteo-dystrophy, small scarred kidney.
2: Once ARF is established identify the
cause of ARF, eliminate the triggering insult (nephrotoxin) and/or institution of disease specific therapies, prevention and management of uremic complications
Clinical assessment Prerenal ARF: Thirst, orthostatic dizziness, tachycardia, reduced jugular venous pressure, decreased skin turgor, dry mucous membrane, reduced axillary sweating, Intrinsic renal ARF: Ischemic and nephrotoxic causes should be ruled out which constitute 90% of causes Post renal ARF: Suprapubic and flank pain, colicky pain, Neurogenic bladder should be ruled out in patients on anticholinergic.
Urine analysis Anuria suggests complete urinary tract obstruction Prerenal: contains transparent hyaline casts formed in concentrated urine from normal constituents of urine mainly Tamm-Horsfall protein secreted by the epithelial cells of the loop of Henle.
Labarotary findings: Creatinine: peak creatinine is observed
after 3-5 days after contrast nephropathy, and 7-10 days after ischemic ARF and athero embolic disease. Hyperkalemia, hyperphosphatemia, hypocalcemia, increased uric acid, and creatinine kinase at the time of presentation suggests diagnosis of rhabdomyolisis.
Hyperurecemia > 15mg/dL in association with hyperkalemia, hyperphophatemia, and raised levels of LDH indicate acute urate nephropathy and tumor lysis syndrome following chemotherapy. Radilogy: Renal biopsy
Complications ARF impairs renal excretion of Na, K, and water, disturbs divalent cation homeostasis and urinary acidification mechanisms. Hence ARF presents with intravascular volume overload, hyponatremia, hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, and metabolic acidosis, rise in nitrogenous waste products leading to uremic syndrome
Expansion of Extracellular fluid volume: Diminished salt and water excretion in oliguric or anuric patients is characterized by weight gain Bilateral basal crepts Raised JVP Dependent edema Pulmonary edema Cerebral edema Neurologic abnormalities including seizures
Hyperkalemia Serum K rises by 0.5 mmol/L per day in oliguric and anuric patients due to impaired excretion of ingested or infused K and K released from the injured tissue. Coexisting metabolic acidosis will exaggerate hyperkalaemia by promoting K efflux from cells. Metabolism of dietary protein yields 50-100 mmol/d of fixed non volatile acids. Mild hyperphosphatemia is always seen in ARF, and also in patients with rhabdomyolysis, hemolysis, tumor lysis. Metastatic deposition of calcium phosphate leads to hypocalcemia.
Anemia: is due to impaired erythropoesis, hemolysis, bleeding, hemodilution, and reduced red cell survival time Increased bleeding time, leukocytosis. Infection Cardiopulmonary complications GIT bleeding Uremic syndrome
TREATMENT
Prevention: No specific therapy for ischemic or nephrotoxic ARF except preventing the etiologic factors. Preventing hypotension by aggressive volume replacement Judicious use of nephrotoxic drugs Adjusting dosage of the nephrotoxic drugs
Allupurinol and forced alkaline diuresis in patients at high risk of urate nephropathy (cancer chemotherapy, hematologic malignancies) N-acetylcysteine limits acetaminophen induced injury Dimercaprol prevents the metal nephrotoxicity
Specific therapies Prerenal: Correction of hypovolemia depends upon the etiology that has caused it. Corrected with blood if it is due to hemorrhage Isotonic saline is appropriate replacement for mild to moderate hemorrhage or plasma loss. Serum K and acid base status should be corrected
Cardiac failure needs aggressive
management with positive ionotropes, preload and afterload reducing agents, antiarrhythmic agents, IABP. Fluid management may be difficult in patients with cirrhosis and ascites. Hepatorenal syndrome should be ruled out
Intrinsic renal ARF ANP therapy Low dose dopamine Loop diuretic Calcium channel blockers Alpha adreno-receptor blocker Prostaglandin analogues
Antioxidants Antibodies against leukocyte adhesion molecules Insulin like growth factors ARF due to glomerulonephritis, and vasculitis respond better with glucocorticoids, alkylating agents, and plasma pheresis Hypertension and ARF due to scleroderma is sensitive to ACE inhibitors
Post Renal ARF Can be detected by collaboration of nephrologists, urologist, and radiologist. Obstruction of the urethra and bladder neck is managed initially by catheterization. Supportive measures: Salt water intake is titrated as required Diuretics to correct hypovolemia Management of hyperkalemia Correction of metabolic acidosis
Hyperphosphatemia is corrected by
Alluminium hydroxide, calcium carbonate Nutrition therapy to prevent the catabolism and starvation ketoacidosis, by restricting the protein intake to 0.6g/kg, and giving high carbohydrate diet Blood transfusion if anemia Dialysis
Outcome and long term prognosis
Mortality rate with ARF is about 50%,
patients usually die of the sequelae of primary illness that lead to ARF and not ARF per say. Patients with oliguria UOP< 400ml/d and rise in serum creatinine > 3mg/dl at the time of admission have a poor prognosis
Acute renal failure (ARF) is a syndrome
characterized by rapid decline in GFR hours to days, retention of nitrogenous waste products and disturbances in the extra cellular volume, electrolyte and acid base homeostasis.
Is seen as a complication in about 5% of hospital admissions, and up to 30% of intensive care admissions. Oliguria is a common finding but not necessary. ARF is sometimes asymptomatic and is diagnosed by increase in the urea and creatinine.
CLASSIFICATION AND MAJOR CAUSES OF ACUTE RENAL FAILURE (ARF)
I: PRERENAL ARF: A: Hypovolemia 1: Hemorrhage, burns, dehydration 2: GIT fluid loss; vomiting, surgical drainage, diarrhea 3: Renal fluid loss; diuretics, osmotic diuresis (Diabetes mellitus), hypoadrenalism 4: Sequestration in extravascular space; pancreatitis, peritonitis, trauma, burns, severe hypoalbuminemia
B: Low cardiac output: 1: Diseases of myocardium, valves, and pericardium, arrhythmias, tamponade 2: Other: pulmonary hypertension, massive pulmonary embolus, positive pressure mechanical ventilation
C: Altered Renal systemic vascular resistance ratio 1: Systemic vasodilation; Sepsis, antihypertensives, afterload reducers, anesthesia, anaphylaxis 2: Renal vasoconstriction: Hypercalcemia, norepinephrine, epinephrine, cyclosporine, FK 506, amphoterecin B 3: Cirrhosis with ascites (hepatorenal syndrome)
D: Renal hypoperfusion: with impairement of renal autoregulatory responses 1: Cyclooxygenase inhibitors, ACE inhibitors E: Hyperviscosity syndrome 1: Multiple myeloma, macroglobenemia, polycythemia
II: INTRINSIC RENAL ARF 1: Reno-vascular obstruction (Bilateral or unilateral in the setting of one functioning kidney) A: Renal artery obstruction: Atherosclerotic plaque, thrombosis, embolism, dissecting aneurysms, vasculitis B: Renal vein obstruction: Thrombosis, compression
2: Diseases of the glomeruli or renal
microvasculature
A: Glomerulo nephritis and vasculitis B: Hemolytic uremic syndrome: Thrombotic thrombocytopenic purpura, DIC, toxemia of pregnancy, accelerated hypertension, radiation nephritis, SLE, scleroderma
3: Acute tubular necrosis: A: Ischemia: As per pre-renal ARF, Obstetric complications (abruption placenta, post partum hemorrhage) B: Toxins: 1: Exogenous: radio contrast, cyclosporine, antibiotics (aminoglycosides), chemotherapy (cisplatin), organic solvents (Ethylene glycol), acetaminophen, illegal abortificients 2: Endogenous: Rhabdomyolysis, hemolysis, uric acid, oxalate, plasma cell dyscrasia (myeloma)
4: Interstitial nephritis
A: Allergic; Antibiotics (beta lactums, sulfonamides, trimethoprim, rifampicin), NSAID, diuretics, captopril B: Bacterial; (acute pyelonephritis, leptospirosis), viral (cytomegalovirus), fungal (candidiasis) C: Infiltration: Lymphoma, leukemia, sarcoidosis. D: Idiopathic: 5: Intratubular deposition and obstruction Myeloma proteins, uric acid, oxalate, acyclovir, methotrexate, sulphonamides 6: Renal allograft rejection
III: POST RENAL ARF (OBSTRUCTION)
1: Ureteric: Calculi, blood clot, sloughed papillae, cancer, external compression (retroperitoneal fibrosis) 2: Bladder neck ; Neurogenic bladder, Prostatic hypertrophy, calculi, cancer, blood clot 3: Urethra: stricture, Congenital valve, phimosis
Clinical features and differential diagnosis 1: Determine whether decline in GFR it is acute or chronic. Findings that suggest of chronic renal failure are anemia, neuropathy, and radiologic evidence of osteo-dystrophy, small scarred kidney.
2: Once ARF is established identify the
cause of ARF, eliminate the triggering insult (nephrotoxin) and/or institution of disease specific therapies, prevention and management of uremic complications
Clinical assessment Prerenal ARF: Thirst, orthostatic dizziness, tachycardia, reduced jugular venous pressure, decreased skin turgor, dry mucous membrane, reduced axillary sweating, Intrinsic renal ARF: Ischemic and nephrotoxic causes should be ruled out which constitute 90% of causes Post renal ARF: Suprapubic and flank pain, colicky pain, Neurogenic bladder should be ruled out in patients on anticholinergic.
Urine analysis Anuria suggests complete urinary tract obstruction Prerenal: contains transparent hyaline casts formed in concentrated urine from normal constituents of urine mainly Tamm-Horsfall protein secreted by the epithelial cells of the loop of Henle.
Labarotary findings: Creatinine: peak creatinine is observed
after 3-5 days after contrast nephropathy, and 7-10 days after ischemic ARF and athero embolic disease. Hyperkalemia, hyperphosphatemia, hypocalcemia, increased uric acid, and creatinine kinase at the time of presentation suggests diagnosis of rhabdomyolisis.
Hyperurecemia > 15mg/dL in association with hyperkalemia, hyperphophatemia, and raised levels of LDH indicate acute urate nephropathy and tumor lysis syndrome following chemotherapy. Radilogy: Renal biopsy
Complications ARF impairs renal excretion of Na, K, and water, disturbs divalent cation homeostasis and urinary acidification mechanisms. Hence ARF presents with intravascular volume overload, hyponatremia, hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesemia, and metabolic acidosis, rise in nitrogenous waste products leading to uremic syndrome
Expansion of Extracellular fluid volume: Diminished salt and water excretion in oliguric or anuric patients is characterized by weight gain Bilateral basal crepts Raised JVP Dependent edema Pulmonary edema Cerebral edema Neurologic abnormalities including seizures
Hyperkalemia Serum K rises by 0.5 mmol/L per day in oliguric and anuric patients due to impaired excretion of ingested or infused K and K released from the injured tissue. Coexisting metabolic acidosis will exaggerate hyperkalaemia by promoting K efflux from cells. Metabolism of dietary protein yields 50-100 mmol/d of fixed non volatile acids. Mild hyperphosphatemia is always seen in ARF, and also in patients with rhabdomyolysis, hemolysis, tumor lysis. Metastatic deposition of calcium phosphate leads to hypocalcemia.
Anemia: is due to impaired erythropoesis, hemolysis, bleeding, hemodilution, and reduced red cell survival time Increased bleeding time, leukocytosis. Infection Cardiopulmonary complications GIT bleeding Uremic syndrome
TREATMENT
Prevention: No specific therapy for ischemic or nephrotoxic ARF except preventing the etiologic factors. Preventing hypotension by aggressive volume replacement Judicious use of nephrotoxic drugs Adjusting dosage of the nephrotoxic drugs
Allupurinol and forced alkaline diuresis in patients at high risk of urate nephropathy (cancer chemotherapy, hematologic malignancies) N-acetylcysteine limits acetaminophen induced injury Dimercaprol prevents the metal nephrotoxicity
Specific therapies Prerenal: Correction of hypovolemia depends upon the etiology that has caused it. Corrected with blood if it is due to hemorrhage Isotonic saline is appropriate replacement for mild to moderate hemorrhage or plasma loss. Serum K and acid base status should be corrected
Cardiac failure needs aggressive
management with positive ionotropes, preload and afterload reducing agents, antiarrhythmic agents, IABP. Fluid management may be difficult in patients with cirrhosis and ascites. Hepatorenal syndrome should be ruled out
Intrinsic renal ARF ANP therapy Low dose dopamine Loop diuretic Calcium channel blockers Alpha adreno-receptor blocker Prostaglandin analogues
Antioxidants Antibodies against leukocyte adhesion molecules Insulin like growth factors ARF due to glomerulonephritis, and vasculitis respond better with glucocorticoids, alkylating agents, and plasma pheresis Hypertension and ARF due to scleroderma is sensitive to ACE inhibitors
Post Renal ARF Can be detected by collaboration of nephrologists, urologist, and radiologist. Obstruction of the urethra and bladder neck is managed initially by catheterization. Supportive measures: Salt water intake is titrated as required Diuretics to correct hypovolemia Management of hyperkalemia Correction of metabolic acidosis
Hyperphosphatemia is corrected by
Alluminium hydroxide, calcium carbonate Nutrition therapy to prevent the catabolism and starvation ketoacidosis, by restricting the protein intake to 0.6g/kg, and giving high carbohydrate diet Blood transfusion if anemia Dialysis
Outcome and long term prognosis
Mortality rate with ARF is about 50%,
patients usually die of the sequelae of primary illness that lead to ARF and not ARF per say. Patients with oliguria UOP< 400ml/d and rise in serum creatinine > 3mg/dl at the time of admission have a poor prognosis
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