Intrinsic Renal Failure Diagnosis

Intrinsic Renal Failure Diagnosis

During acute intrinsic renal failure, three clinical phases can be distinguished. The initial phase of injury is the period between the onset of insult and established renal failure. This phase can last several hours or, rarely, days. The second phase is that of established renal failure or the maintenance phase, characterized by reduction of the GFR and azotemia. This phase usually lasts several days to weeks. Oliguria that lasts more than 90 days often indicates the possibility of residual structural impairment.

The third or recovery phase results in a gradual increase in GFR and diuresis. An increase in urine output will improve the fluid and electrolyte imbalance. Glomerular filtration recovers more rapidly than tubular function, and the patient may demonstrate a lengthy period of tubular dysfunction, such as an inability to concentrate urine and increased salt losses. Recovery may extend over several weeks to months; the usual time of renal recovery is about 30 days.

A history may help in establishing the etiology of intrinsic renal failure. Edema, skin infection, or smoky urine suggests postinfection glomerulonephritis; purpuric rash, abdominal pain, and diarrhea suggest vasculitis; and urticarial rash, use of drugs, fever, and arthralgia may indicate acute interstitial nephritis. Once the kidney has developed intrinsic renal failure, the signs and symptoms usually are independent of the etiology. Nonspecific generalized symptoms (lethargy, anorexia, vomiting, abdominal pain) can be present. Signs of fluid retention (peripheral and pulmonary edema, hypertension) and changes in urine pattern (oliguria, anuria, or polyuria) are prominent. The hallmark of intrinsic renal failure is the worsening of azotemia, with a daily rise in serum creatinine (0.5 to 1.5 mg/dL) and in BUN (10 to 20 mg/dL).

Hyponatremia frequently is dilutional, secondary to fluid retention and/or to the administration of hypotonic solutions. Hyperkalemia develops primarily as the result of decreased GFR and cellular catabolism. Metabolic acidosis results from the reduced capacity of the kidneys to regulate acid base homeostasis and lactic acid accumulation. Hyperphosphatemia develop secondary to decreased filtration as well as cell destruction. Low serum calcium is secondary to hyperphosphatemia, resistance to parathyroid hormone, and abnormalities in vitamin D metabolism. Usually, hypocalcemia is asymptomatic, but can lead to tetany, convulsions, or hypotension. The uric acid level may become markedly elevated during the oliguric phase.

Anemia is a result of the dilution, decreased erythropoiesis, hemolysis, and blood loss. Leukopenia or leukocytosis can be evident. Microangiopathic hemolytic anemia (Coombs negative) with fragmented erythrocytes on the peripheral smear and thrombocytopenia are characteristics of hemolytic-uremic syndrome. Coagulation abnormalities accompanied by an increase in bleeding time secondary to the platelet dysfunction are found in severe uremia.

Proteinuria of more than 1 g/d, numerous dysmorphic red blood cells, and red blood cell and granular casts are seen in glomerulonephritis and vasculitis. In the case of acute interstitial nephritis, pyuria, eosinophiluria, scant casts (mainly white blood cell casts), and tubular cells are present. Myoglobinuria or hemoglobinuria should be suspected whenever there exists a urine sample that has blood on the dipstick and only 1 to 2 red blood cells in the sediment. Urinary sediment with numerous coarse granular or pigmented casts and/or tubular cells are characteristic of ATN. Urinary indices will reflect tubular dysfunction and injury and will document the inability of the kidney to concentrate urine and conserve sodium (a urine osmolality <350 mOsm/kg H2O, urine Na >40 mEq/L, FENa >2.5%).

Renal ultrasonography usually shows enlarged kidneys with a uniform increased cortical echogenicity; a renal scan shows poor uptake and excretion of radioisotope.



image source: http://en.wikipedia.org/wiki/Acute_kidney_injury

Title Post: Intrinsic Renal Failure Diagnosis
Rating: 100% based on 99998 ratings. 5 user reviews.
Author: Unknown

Thanks for visiting the blog Family Medical Center, If there are criticisms and suggestions please leave a comment

Advertisement