Renal failure is the inability of the kidneys to carry out their normal functions, including urine formation and excretion, acid-base and electrolyte balance, and hormone-related functions such as vitamin D metabolism and erythropoietin synthesis. It may be:

• Acute, developing over hours to days
• Chronic, developing over years

Acute renal failure may be reversible with treatment, while chronic renal failure is usually irreversible. In end-stage renal disease (ESRD), renal function has been irreversibly lost, and the patient becomes dependent on renal replacement therapy (dialysis or renal transplantation) to survive.

Acute kidney injury or AKI: Previously called acute renal failure, AKI is an abrupt decrease in renal function. It is characterized by:

• An acute rise in serum creatinine (> 1.5 times the baseline)
• An acute decrease in GFR
• Anuria or oliguria (< 0.5 ml/kg/hour for at least 6 hours)

Depending on the etiology, AKI 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 works best when you can identify the cause and type of AKI, although this may not be clear early on. Patients without pre-existing renal disease generally have a better prognosis in the setting of AKI.

Key management principles include maintaining adequate renal perfusion while also assessing for volume overload. Volume status can be evaluated using clinical signs and by measuring central venous pressure (CVP). Isotonic crystalloid solutions such as 0.9% normal saline and Ringer’s lactate are preferred. Diuretics can be used for fluid overload.

Electrolytes should be monitored closely, especially for hyperkalemia. Severe hyperkalemia is treated with insulin with dextrose, calcium gluconate, Kayexalate resin, and loop diuretics. Avoid nephrotoxic agents such as intravenous contrast and metformin. Dialysis is needed in some cases.

Chronic renal disease or CKD: CKD 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 initially compensates for decreased function through hyperfiltration and hypertrophy of the remaining nephrons. Over time, progressive structural damage develops, including fibrosis, distortion of glomerular architecture, sclerosis of blood vessels, abnormal podocyte function and podocyte loss, increased deposition of extracellular matrix, and tubulointerstitial fibrosis.

Common associated findings include hyperphosphatemia, secondary hyperparathyroidism and renal osteodystrophy, osteopenia, normocytic normochromic anemia, hyperkalemia, and metabolic acidosis.

Management is supportive, focusing on control of the underlying conditions and renal replacement therapy when needed. Some patients may progress to ESRD.