genitourinary disorders
Acute Kidney Injury (AKI)
Etiology of AKI
Causes of acute kidney injury (AKI; see table) can be classified as Prerenal Renal Postrenal Prerenal AKIis due to inadequate renal perfusion. The main causes are Extracellular fluid Volume Depletion (eg, due to inadequate fluid intake, diarrheal illness, Cardiovascular disease (eg, Heart Failure (HF) , Decompensated liver disease Prerenal conditionstypically do not cause permanent kidney damage (and hence are potentially reversible) unless hypoperfusion is severe and/or prolonged. Hypoperfusion of an otherwise functioning kidney leads to enhanced reabsorption of sodium and water, resulting in oliguria (urine output<500 mL/day) with high urine osmolality and low urine sodium. Renalcauses of AKI involve intrinsic kidney disease or damage. Disorders may involve the blood vessels, glomeruli, tubules, or interstitium. The most common causes are Acute Tubular Necrosis (ATN) None Overview of Nephritic Syndrome None Nephrotoxins (including prescription and over-the-counter drugs—see Analgesic Nephropathy ) Glomerular disease reduces glomerular filtration rate (GFR) and increases glomerular capillary permeability to proteins and red blood cells; it may be inflammatory (glomerulonephritis) or the result of vascular damage due to ischemia or vasculitis. Tubules also may be damaged by ischemia and may become obstructed by cellular debris, protein or crystal deposition, and cellular or interstitial edema. Interstitial inflammation ( Tubulointerstitial Nephritis ) usually involves an immunologic or allergic phenomenon. These mechanisms of tubular damage are complex and interdependent, rendering the previously popular term acute tubular necrosis an inadequate description. ( Obstructive Uropathy ) is due to various types of obstruction in the voiding and collecting parts of the urinary system. Obstruction can also occur on the microscopic level within the tubules when crystalline or proteinaceous material precipitates. Obstructed ultrafiltrate, in tubules or more distally, increases pressure in the urinary space of the glomerulus, reducing GFR. Obstruction also affects renal blood flow, initially increasing the flow and pressure in the glomerular capillary by reducing afferent arteriolar resistance. However, within 3 to 4 hours, the renal blood flow is reduced, and by 24 hours, it has fallen to<50% of normal because of increased resistance of the renal vasculature. Renovascular resistance may take up to a week to return to normal after relief of a 24-hour obstruction. To produce significant AKI, obstruction at the level of the ureter requires involvement of both ureters unless the patient has only a single functioning kidney. Bladder outlet obstruction due to an Benign Prostatic Hyperplasia (BPH) is probably the most common cause of sudden, and often total, cessation of urinary output in men. 