Acute Renal Failure (ARF):

KIDNEY DISEASES

ACUTE RENAL FAILURE:

There is sudden decline in renal function leading to retention of nitrogenous and other waste products, disordered H⁺ ion homeostasis and imbalance in ECF volume and composition (dilutional hyponatraemia, retention of sodium and water, hyperkalaemia due to retention of potassium). In ARF the impairment is reversible unlike CRF which is irreversible and develop over a period of years.

ARF is classified into prerenal (due to impaired renal perfusion), renal (within the kidney) and postrenal (obstructive) causes.

Prerenal renal failure:

 

This is characterized by normal renal structure, normal tubular function and rapid reversibility after management. It is a consequence of reduced renal perfusion may be due to cardiovascular insufficiency (hypovolaemia and hypotension), diuresis, cardiogenic shock, GI fluid loss, burns, CHF, or derangement of intrarenal haemodynamics.

Laboratory findings are increased plasma urea disproportionately to creatinine because due to hypoperfusion more urea is diffused back as urine flow rate falls.

Urinalysis shows hyaline casts and there is no proteinuria.

There is low sodium in urine due to more absorption induced by hypovolaemia (<20 mmol/L), urine osmolality/plasma osmolality is >1.5, urine urea/plasma urea is >10.

Intrinsic renal failure:

 

It can progress from prerenal cause but other conditions are present like nephrotoxins like NSAID, intrinsic renal disease (glomerulonephritis), speticaemia, hypercalcaemia, sarcoidosis (infiltrative disorder), etc. Acute tubular necrosis is used synonymously used with intrinsic ARF.

Presence of proteinuria, urine sodium >40 mmol/L, urine urea/plasma urea <5, urine osmolality/plasma osmolality <1.1.  Urea and creatinine concentration in plasma rise in parallel.

Urinalysis shows high epithelial cells free or in the form of cast, hematuria and red cell cast are present in glomerulonephritis.

Acute tubular necrosis (ATN):  

The causes of ATN are continued vasoconstriction occurring due to intrarenal release of vasoactive substances like endothelin and prostaglandins, and angiotensin II (renin secretion may remain high secondary to decreased delivery of solute especially sodium to the macula densa or due to hypovolaemia). This vasoconstriction reduces the renal perfusion producing tubular necrosis. Also nephrotoxins can cause necrosis. This necrosis also obstructs urine flow and impairs tubular sodium reabsorption leading to oliguria and secondary release of renin that further produce vasoconstriction respectively. Direct damage to the glomeruli results in decreased filtration, and physical obstruction of lumens of nephrons by swollen tubular cells or tubular debris.

Obstructive (postrenal) renal failure:

The common causes are ureteric obstruction by calculi, tumors, urethral stricture, prostate carcinoma, etc. There is oliguria or sometimes anuria in severe cases.

Plasma Na is low due to dilutional hyponatraemia. Hyperkalaemia is life threatening complication of ARF and may indicate renal replacement treatment (if plasma potassium >7.0 mmol/L). Potassium increases due to decreased renal excretion, acidosis and loss of intracellular potassium to ECF.

Patients with ARF are acidotic and this is due to loss of bicarbonate, retention of hydrogen ions and this requires further medical management.