RENAL FAILURE

Renal failure occurs in either an acute or chronic form. The acute form most often occurs because of a sudden body insult such as severe dehydration; think: lost in the desert. Other causes of acute renal failure include prolonged anesthesia, hemorrhage, shock, severe diarrhea, or sudden traumatic injury. It can also occur during cardiopulmonary bypass when having heart surgery, or because of aminoglycosides, penicillin, cephalosporins, and sulfonamides, or because of poisons (arsenic) or industrial waste exposure such as mercury. All of these conditions cause ischemia which ultimately leads to acute renal failure. The chronic form of renal failure occurs from 1) developmental abnormalities, 2) when acute becomes long-term, 3) chronic causes extensive nephron damage/destruction. The nephrons that are NOT destroyed function normally, they are simply inadequate in number to sustain kidney function. Glomeruli can adjust so that kidney function can continue until 50% of nephrons are destroyed. After that point, kidney function diminishes by degrees until ESRD (end-stage renal disease). HOW IT ALL BEGINS One of the 1st symptoms noted with acute renal failure is oliguria, output of 1 mL/kg per hour. Azotemia (nitrogen waste build up) will occur because of oliguria; this is the stage of nitrogen waste building. Next comes Uremia: this is when nitrogen waste has actually built up in the blood, possibly causing additional toxic symptoms such as cerebral irritation. BUN will begin to rise progressively as renal insufficiency continues and the breakdown products of protein cannot be excreted. A BUN level greater than 80 to 100 mg/100 mL is toxic and must be corrected (dialysis). Your liver produces ammonia which contains nitrogen after it breaks down proteins used by your body's cells. The nitrogen combines with other elements, such as carbon, hydrogen and oxygen, to form urea, which is a chemical waste product. The urea travels from your liver to your kidneys through your bloodstream. Healthy kidneys filter urea and other waste products from your blood. The filtered waste products leave your body in urine only with proper kidney function. Creatinine, is a break-down product of creatinine-phosphate in muscle, and is usually produced at a fairly constant rate by the body (depending on muscle mass). Creatinine is chiefly filtered out of the blood by the kidneys (glomerular filtration and proximal tubular secretion). There is little to no tubular reabsorption of creatinine. If the filtering of the kidney is deficient, creatinine

blood levels rise. Therefore, creatinine levels in blood and urine may be used to calculate the creatinine clearance (CrCl), which reflects the glomerular filtration rate (GFR). Because creatinine is normally excreted at a uniform rate, a rate of less than 10:100 indicates severe renal failure. As the kidneys become unable to dilute or concentrate urine, the specific gravity becomes fixed at 1.010. Hyperkalemia may occur as kidney filtration progressively declines. Manifestations such as a weak, irregular pulse, abdominal cramps, lowered BP, and muscle weakness occur Acidosis will follow shortly due to an inability to excrete H+ ions. When total output decreases, phosphorus levels will rise and deplete calcium serum levels because phosphorus and calcium have inverse properties. The failing kidneys are no longer good at getting rid of excess phosphorus and the levels in the blood begin to rise. The rise in phosphorus upsets the delicate balance between calcium and phosphorus and activates a regulatory hormonal cascade which attempts to re-establish control. Without healthy kidney tissue to play its role in this balance, the body is fighting a losing battle. Calcium is mobilized from bone to balance the phosphorus but in the end this only serves to demineralize and weaken the bones and cause calcium phosphate deposits to form in soft tissues. Bone growth ceases. Hypocalcemia leads to a condition renal osteodystrophy and tetany. As nephron loss continues, the kidneys cannot concentrate urine, resulting in polyuria and may be manifested as enuresis. Acute renal failure becomes chronic renal failure. CHRONIC RENAL FAILURE The few functioning nephrons cannot reabsorb enough sodium to maintain a proper level of body fluid; dehydration occurs. Eventually urine is retained and edema occurs as well as hypertension because the kidneys can barely control the blood pressure at this point. The kidneys are responsible for synthesis of vitamin D to its active form (calcitrol). With poor kidney function, vitamin D cannot be used, calcium cannot be absorbed from the GI tract, and renal rickets occurs. Erythropoieten, formed by the kidneys, stimulates red bood cell production; RBC production is severely decreased and anemia develops. As a result of progressive failure, pruritis presents as skin is irritated due to excretion of wastes in sweat from high levels of BUN and creatinine.