Articles on Medical Diseases and Conditions

Tag: Kidney

  • Kidney

    Renal cell adenocarcinoma (hypernephroma) is about twice as frequent in males as in females. It occurs with about equal frequency in both kidneys. About 90% of cases occur after age 40, although more than 30 cases have been reported in children. About 80% of renal cell carcinomas are located in either the upper or the lower poles of the kidney.

    Clinical findings. In renal cell adenocarcinoma, symptoms and urinary findings vary according to the location, size, and aggressiveness of the tumor. Renal carcinoma often causes hematuria (as does bladder carcinoma). Painless gross hematuria is the initial symptom in about 40% of patients and occurs with other symptoms in additional cases. These episodes are often intermittent and may be misdiagnosed as urinary tract calculus or infection. Flank pain is present in about 40% of patients, and about one third have a significant degree of weight loss. A mass is noticeable to the patient in about 10%–15% of cases and is palpable by the physician in about 50% of cases. In addition, hypernephroma, on occasion, is a well-recognized cause of fever of unknown origin. It has rarely but repeatedly been associated with secondary polycythemia (about 3% of patients), although a large minority have anemia and the majority do not show hemoglobin abnormality. About 20% of patients have hypertension (range, 4%–38%). About 10% (range, 4%–28%) have no clinical symptoms suggestive of hypernephroma, and the tumor is discovered on intravenous pyelogram (IVP) performed for some other reason.

    Laboratory findings. Hematuria, either gross or microscopic, is the most frequent abnormality, being detected at some time in about 60% of patients (range, 28%–80%). Unfortunately, most publications either do not differentiate between gross and microscopic hematuria or record gross hematuria only. In 38 patients with renal cell adenocarcinoma seen in my area, 39% had gross hematuria and an additional 27% had microscopic hematuria. Proteinuria may be present but is less frequent. About 30% of patients have a completely normal urinalysis on admission. The IVP is the most useful screening test for renal cell carcinoma and, if carefully done, will also detect many cases of carcinoma in the renal pelvis and ureters. Other procedures, such as kidney scanning or computerized tomography (CT), are also useful.

    Other procedures. Once a space-occupying lesion is identified in the kidney, the question arises as to its nature. B-mode ultrasound, CT, and drip infusion tomography seem to be excellent methods of distinguishing a solid renal tumor from a renal cyst. However, there is coincidence of renal carcinoma and simple renal cyst in about 2%–3% (literature range, 2%–7%) of cysts explored. Selective renal angiography is also very effective and can be performed if tomography is inconclusive. No technique is infallible, however, since a few tumors may become exceptionally cystic due to internal necrosis. Urine cytology has relatively little value at present in the diagnosis of renal cell adenocarcinoma. Metastatic carcinoma or malignant lymphoma in the kidney usually does not produce significant clinical or urinary findings.

  • Serum Aspartate Aminotransferase (AST)

    Serum aspartate aminotransferase (AST; formerly SGOT) is an enzyme found in several organs and tissues, including liver, heart, skeletal muscle, and RBCs. AST elevation from nonhepatic sources is discussed elsewhere.

    AST elevation originating from the liver is due to some degree of acute liver cell injury. Following onset of acute hepatocellular damage from any etiology, AST is released from damaged cells. The serum level becomes elevated in approximately 8 hours, reaches a peak in 24-36 hours, and returns to normal in 3-6 days if the episode is short lived. In mild injury, serum levels may be only transiently and minimally elevated or may even remain within reference limits. In acute hepatitis virus, AST levels frequently become elevated more than 10 times the upper reference range limit (about 75% of patients in one study and 100% in another) and typically rise more than 20 times the upper limit (about 45% of patients in the first study and 90% in the second). In fact, a serum AST more than 20 times normal usually includes acute hepatitis virus infection in the differential diagnosis. However, 1-2 weeks later the values fall toward normal, so that a test sample drawn in the subsiding phase may show moderate or possibly only mild abnormality. In extrahepatic obstruction there usually is no elevation unless secondary parenchymal acute damage is present; when elevations occur, they are usually only mild to moderate (<10 times the upper reference limit). However, when extrahepatic obstruction occurs acutely, AST values may quickly rise to values more than 10 times normal, then fall swiftly after about 72 hours. In cirrhosis, whether the AST level is abnormal and (if abnormal) the degree of abnormality seems to depend on the degree of active hepatic cell injury taking place. Inactive cirrhosis usually is associated with normal AST levels. In active alcoholic cirrhosis, AST elevation is most often mild to moderate, with the majority of AST values less than 5 times the upper range limit and over 95% of AST values less than 10 times normal. In active chronic hepatitis virus hepatitis, AST values are also usually less than 10 times normal. However, one group reported that about 15% of their patients had at some time values more than 10 times normal. However, some of these patients could have superimposed acute infection by non-A, non-B or delta hepatitis virus. In liver passive congestion, AST levels are elevated in 5%-33% of patients. About 80% of these patients have AST elevations less than 3 times normal. In severe acute congestive failure, liver hypoxia may be severe, and one study estimated that about 50% of these patients have AST elevation. In some of these patients AST levels may be higher than 3 times normal and occasionally may even exceed 20 times normal (about 1% of patients with substantial degrees of congestive failure). In some cases AST elevation due to acute myocardial infarction adds to AST arising from the liver. In infectious mononucleosis, AST levels are elevated in 88%-95% of patients, but only about 5% of elevations are greater than 10 times normal and about 2% are more than 20 times normal.

    Some Etiologies for Aspartate Aminotransferase Elevation
    Heart
    Acute myocardial infarct
    Pericarditis (active: some cases)
    Liver
    Hepatitis virus, Epstein-Barr, or cytomegalovirus infection
    Active cirrhosis
    Liver passive congestion or hypoxia
    Alcohol or drug-induced liver dysfunction
    Space-occupying lesions (active)
    Fatty liver (severe)
    Extrahepatic biliary obstruction (early)
    Drug-induced
    Skeletal Muscle
    Acute skeletal muscle injury
    Muscle inflammation (infectious or noninfectious)
    Muscular dystrophy (active)
    Recent surgery
    Delirium tremens
    Kidney
    Acute injury or damage
    Renal infarct
    Other
    Intestinal infarction
    Shock
    Cholecystitis
    Acute pancreatitis
    Hypothyroidism
    Heparin therapy (60%-80% of cases)

    There is a large group of common diseases with mild or moderate AST elevation (defined arbitrarily as elevated less than 10 times the upper reference limit); these include acute hepatitis in the subsiding or recovery phases, chronic hepatitis, active cirrhosis or alcoholic liver disease, liver passive congestion, drug-induced liver dysfunction (including intravenous [IV] or subcutaneous heparin), metastatic liver tumor, long-standing extrahepatic bile duct obstruction, infectious mononucleosis, cytomegalovirus (88%-95%; 2% more than 10 times normal), and fatty liver (40%; rare > 5 x normal). As mentioned earlier, in a few patients with active cirrhosis, liver congestion, infectious mononucleosis, and drug-induced liver injury, the AST may attain levels more than 20 times upper reference limit that are suggestive of acute hepatitis virus infection. AST levels are elevated in approximately 50% of patients with liver metastases, with most elevations less than 5 times the upper reference limit. One report found that obese patients had upper reference limits up to 50% higher than normal-weight persons.

    In active alcoholic cirrhosis, liver congestion, and metastatic tumor to the liver, the AST level usually is considerably higher than the alanine aminotransferase (ALT; formerly SGPT) level, with an AST/ALT ratio greater than 1.0. Ratios less than 1.0 (ALT equal to or greater than AST) are the typical finding in acute hepatitis virus hepatitis and infectious mononucleosis. However, about 30% of patients with acute hepatitis virus infection and some patients with infectious mononucleosis have a ratio greater than 1.0; and ratios either greater than or less than 1.0 may occur in patients with AST elevation due to extrahepatic obstruction. The ratio tends to be more variable and less helpful when the AST value is greater than 10 times the upper reference limit. Some prefer to use an AST/ALT ratio of 1.5 or 2.0 rather than 1.0 as the cutoff point (i.e., an AST value more than twice the ALT value is more suggestive of alcoholic active cirrhosis than hepatitis virus hepatitis, especially if the AST value is less than 10 times normal). Although most agree that active alcoholic liver disease usually yields AST values significantly higher than ALT, there is disagreement in the literature on the usefulness of the ratio (especially the 1.0 value) for diagnosis of individual patients.