RENAL FAILUREAcute Renal Failure
Acute renal failure (ARF) is a condition of abrupt deterioration in renal function as evidenced by rising blood urea nitrogen (BUN) and creatinine levels. It is usually associated with decreased urine output. Approximately occur in the surgical setting and early recognition can minimize the extent of renal injury. It is classified under 3 categories: prerenal, postrenal and intrarenal.
Prerenal azotemia is caused by the direct result of inadequate renal blood flow. If the cause for the poor blood flow can be reversed then the problem can be resolved. However, prolonged low flow states can produce ischemic kidney injury.
Causes of Prerenal azotemia:
1) Volume depletion – hemorrhage, dehydration
2) Low cardiac output – congestive heart failure, cardiogenic shock)
3) Renal artery (stenosis, occlusion, vasoconstriction)
4) Systemic vasodilatation (sepsis, anaphylaxis, overdose)
Postrenal azotemia is caused by obstruction to urine flow. Pressures in the renal collecting system and tubules rise with obstruction causing renal injury if the obstruction is not relieved.
Causes of urinary obstruction:
1) Bladder outlet – enlarged prostate, urethral stricture, bladder stones, foreign body, tumor, blood clot)
2) Ureter – stones, tumors, stricture, stenosis
Intrarenal
Acute parenchymal renal failure is the result of damage to the renal tubules brought about by inflammation, injury from substances toxic to the kidney (nephrotoxic) and decreased blood flow.
Causes of intrarenal failure
1) Acute tubular necrosis (ATN) – 3 phases: 1) onset 2) oliguric 3) postoliguric. The oliguric period (urine output less than 500cc/day) typically lasts for 10-14 days but may be as brief as 2 days or as long as 6-8 weeks. A non-oliguric ATN can occur when it is secondary to nephrotoxic injury for ex from certain drugs or substances.
Causes of ATN
a) Ischemic injury – hypotension, cardiogenic or septic shock
b) Nephrotoxins – aminoglycosides, anesthetic agents, iodinated contrast media, NSAIDS
c) Hemoglobinuria (hemoglobin in the urine) or myoglobinuria (muscle cells in the urine)
2) Acute glomelular nephritis (AGN)
3) Acute interstititial nephritis (AIN)
The work up of a patient with sudden elevation of BUN and creatinine, with or without decreased urine output requires a prompt, systematic approach to exclude any reversible pathophysiologic states and remove any potentially nephrotoxic agents. Prerenal and postrenal causes must be excluded before diagnosing intrinsic renal disease.
CHRONIC RENAL FAILUREChronic renal failure (CRF) is caused by a spectrum of diseases resulting in progressive irreversible loss of functioning nephrons ultimately leading to end stage renal disease (ESRD) requiring dialysis or transplantation. The most common causes include:
1) Diabetes mellitus
2) Hypertension
3) Primary and secondary glomerular disease
4) Hereditary renal disease
5) Obstructive uropathy
6) Chronic infection
7) Interstitial nephritis
A wide variety of systemic symptoms are seen and there is a multisystem involvement making management difficult. Symptoms include:
1) Electrolyte imbalance –decreased phosphates, increased potassium
2) Gastrointestinal – nausea, vomiting, anorexia
3) Hematologic –anemia, platelet dysfunction
4) Neurologic –neuropathy, encephalopathy
5) Cardiovascular – increased severity of atherosclerosis, prolonged hypertension
6) Endocrine – abnormal bone metabolism, glucose intolerance
7) Sexual dysfunction
The general management of patients with CRF centers on slowing the progression of functional renal deterioration. There is no effective treatment for most glomerulopathies. Any reversible or controllable factors must be addressed. Once the glomerular filtration rate deteriorates to levels that produce symptoms of ESRD, then dialysis or transplantation becomes the only option
