Renal failure

Renal failure is inability of the kidneys to perform its functions like formation and excretion of urine, acid-base and electrolyte balance, hormone metabolism like Vit D and erythropoietin synthesis etc. It may be acute, happening over a few hours to days or chronic, occurring over a few years. Acute may be reversible with treatment but chronic is usually irreversible. In end-stage renal disease or ESRD, the renal function has been irreversibly lost and the patient becomes dependent on renal replacement therapy like dialysis or renal transplantation to survive.

Acute kidney injury or AKI: Previously called acute renal failure, AKI is an abrupt decrease in renal function characterized by an acute rise in serum creatinine (> 1.5 times the baseline), acute decrease in GFR and anuria or oliguria (< 0.5 ml/kg/hour for at least 6 hours). Depending on the etiology, it may be pre-renal, intrinsic renal or post-renal.

Causes of AKI

Pre-renal causes

• Renal vasoconstriction due to NSAIDS, ACE inhibitors, ARBs, cyclosporine, tacrolimus, cardiorenal syndrome, hepatorenal syndrome, abdominal compartment syndrome, sepsis, shock
• Hypovolemia from blood loss, diarrhea, vomitings, burns, sweating, diuretic overuse, osmotic diuresis

Intrinsic renal causes

• Glomerular and tubulointerstitial disorders like glomerulonephritis, lupus nephritis, ATN, systemic or renal infections, sarcoidosis, medications like cephalosporins, ciprofloxacin, phenytoin, PPIs, NSAIDs, acyclovir etc
• Vascular disorders like renal vein thrombosis, malignant hypertension, renal embolism etc.

Post-renal causes

• BPH
• Neurogenic bladder
• Calculi with hydronephrosis
• Retroperitoneal fibrosis
• Malignancies of bladder, prostate, cervix

Patients may present with fatigue, anorexia, nausea, vomiting, edema, weight gain, changes in level of consciousness, bleeding tendency from platelet dysfunction in uremia, oliguria and anuria. Physical exam may show pericardial or pleural friction rub, asterixis and myoclonus.

Differences between laboratory findings in different types of renal failure

Prerenal

• FeNa* < 1%
• Urine sodium <20 meq/l
• BUN/creatinine ratio > 20:1
• Urine osmolality > 500 mOsm/kg, hypertonic urine
• Hyaline casts may be seen

Intrinsic renal

• FeNa > 2%
• Urine sodium >40 meq/l
• BUN/creatinine ratio < 10:1
• Urine osmolality <350 mOsm/kg, isotonic or dilute urine
• ATN shows muddy brown casts, tubulointerstitial nephritis shows eosinophils in urine, dysmorphic RBCs or RBC casts are seen in glomerulonephritis

Postrenal

• FeNa <1% (acute), > 1% (after few days)
• Urine sodium <20 meq/l (acute), >40 meq/l (after few days)
• BUN/creatinine ratio about 10-20:1
• Urine osmolality mOsm <350 mOsm/kg
• Hyaline casts may be seen

*Diuretics will alter the FeNa (fractional excretion of sodium), in which case FeUrea should be used. FeNa <1 is also seen in contrast nephropathy.

Management is best if the cause and type of AKI can be established, which may not be clear early on. Patients without pre-existing renal disease have better prognosis in the setting of an AKI. Adequate renal perfusion needs to be maintained while volume overload has to be evaluated at the same time (by clinical signs and measuring central venous pressure or CVP). Isotonic crystalloid solutions like 0.9% normal saline and Ringer’s lactate are preferred. Diuretics can be used in fluid overload. Electrolytes should be monitored, especially hyperkalemia. Severe hyperkalemia is treated with insulin with dextrose, calcium gluconate, Kayexalate resin and loop diuretics. All nephrotoxic agents should be avoided like intravenous contrast, metformin etc. Dialysis is needed in some cases.

Chronic renal disease or CKD: It is persistent impairment of renal function with eGFR < 60ml/min/1.73 m2, lasting for > 3 months. Common causes include diabetes mellitus, hypertension, glomerulonephritis, vasculitis, polycystic kidney disease, VUR, chronic tubulointerstitial nephritis, chronic obstructive uropathy etc. Patients present with non-specific symptoms such as anorexia, fatigue, nausea, vomiting, oliguria, pruritus, refractory hypertension etc. In CKD, the kidney tries to compensate for decreased function by hyperfiltration and hypertrophy of remaining nephrons. Ultimately, fibrosis, distortion of glomerular architecture, sclerosis of blood vessels, abnormal podocyte function and podocyte loss, increased deposition of extracellular matrix and tubulointerstitial fibrosis occurs. Hyperphosphatemia, secondary hyperparathyroidism and renal osteodystrophy, osteopenia, normocytic normochromic anemia, hyperkalemia and metabolic acidosis are seen. Management is supportive, controlling the underlying conditions and renal replacement therapy when needed. Some patients may progress to ESRD.