Articles on Medical Diseases and Conditions

Tag: Weil’s disease

  • Leptospirosis

    Leptospirosis is caused by several species of Leptospira organisms found most often in rats but sometimes present in some farm animals and in some cats and dogs (presumably from rat-transmitted infection). Transmission is most often through accidental contact with water contaminated by infected rat urine. Those most at risk are sewer workers and slaughterhouse employees, but farmers and campers sometimes come into contact with contaminated water. There is an incubation period of 4-20 days, then abrupt onset of fever, often accompanied by chills, headache, malaise, and conjunctivitis. Muscle pain is present in 50% of cases. The fever typically lasts 4-9 days. WBC count can be normal or elevated. Urinalysis often contains protein and some WBCs. Serum bilirubin is usually normal, but about 10% of cases have mild elevation. Alanine aminotransferase is elevated in about 50% of cases, usually to less than five times normal. About 50% of patients experience a recurrence of fever about 1 week (range, 2-10 days) after the end of the first febrile period. Patients are more likely to demonstrate signs of hepatitis in this phase and may develop symptoms of meningitis. The most severe form of leptospirosis is called Weil’s disease and occurs in about 5% of infections. The most striking findings are a combination of hepatitis and glomerulonephritis, clinically manifested by jaundice with hematuria. Therefore, the disease is sometimes considered in the differential diagnosis of jaundice of unknown etiology. Symptoms of meningitis occasionally predominate. Laboratory findings include leukocytosis with a shift to the left. A mild normocytic-normochromic anemia usually develops by the second week. Platelet counts are normal. After jaundice develops, liver function test results are similar to those in viral hepatitis. After onset of kidney involvement, the blood urea nitrogen (BUN) level is often elevated, and hematuria is present with proteinuria. CSF examination shows normal glucose levels but increased cell count, which varies according to the severity of the case; initially, these are mainly neutrophils, but later, lymphocytes predominate. Cultures on ordinary bacterial media are negative.

    Diagnosis often requires isolating the organisms or demonstrating specific antibodies in the serum. During the first week (days 1-8), spirochetes may be found in the blood by dark-field examination in about 8% of cases and can be cultured from the blood in many more. Instead of ordinary blood cultures, one to three drops of blood are inoculated into a special culture medium (Fletcher’s), since larger quantities of blood inhibit the growth of leptospires. The CSF may be cultured toward the end of the first week. During the second week the blood results quickly become negative. During the third week (days 14-21) the spirochetes may often be recovered from the urine of patients with nephritis. Animal inoculation is the most successful method. Antibodies start to appear at about day 7 and are present in most cases by day 12. Antibodies persist for months and years after cure. A titer of 1:300 is considered diagnostic, although without a rising titer, past infection cannot be ruled out completely. If a significant titer has not developed by day 21, it is very rare for it to do so later. In summary, blood cultures during the first week and serologic tests during the second and third weeks are the diagnostic methods of choice.

  • Urinalysis in Miscellaneous Diseases

    Fever. Fever is the most common cause of proteinuria (up to 75% of febrile patients). If severe, it may be associated with an increase in hyaline casts (etiology unknown, possibly dehydration).

    Cystitis-urethritis. Cystitis and urethritis are lower urinary tract infections, often hard to differentiate from renal infection. Clumping of WBCs is suggestive of pyelonephritis but only WBC casts provide absolute specificity. Necrotizing cystitis may cause hematuria. The two-glass urine test helps to differentiate urethritis from cystitis. After cleansing the genitalia, the patient voids about 10-20 ml into container number 1 and the remainder into container number 2. A significant increase in the WBC count of container number 1 over that of container number 2 suggests urethral origin.

    Genitourinary tract obstruction. Neuromuscular disorders of the bladder, congenital urethral strictures and valves, intrinsic or extrinsic ureteral mechanical compressions, and intraluminal calculi produce no specific urinary changes but predispose to stasis and infection. Obstruction, partial or complete, is a frequent etiology for recurrent genitourinary tract infections.

    Amyloidosis. Renal involvement usually leads to proteinuria. In a minority of cases, when the process severely affects the kidney there may be high proteinuria and sediment typical of the nephrotic syndrome. The urinary sediment, however, is not specific, and RBC casts are not present. Renal amyloidosis is usually associated with chronic disease, such as long-standing osteomyelitis or infection, or multiple sclerosis.

    Urinary calculi. Urinary calculi often cause hematuria of varying degree and, depending on the composition of the stone, may be associated with excess excretion of calcium, uric acid, cystine, phosphates, or urates in the urine, even when calculi are not clinically evident. Frequent complications are infections or obstruction, and infection may occur even in the absence of definite obstruction. Ureteral stone passage produces hematuria, often gross. Intravenous pyelography is the best means of diagnosis. Some types of calculi are radiopaque, and others may be localized by finding a site of ureteral obstruction.

    Sickle cell anemia. Hematuria frequently occurs due to kidney lesions produced by intra-capillary RBC plugs, leading to congestion, small thromboses, and microinfarctions. Hematuria is also frequent at times of hematologic crises. Hematuria may be present even without crises in sickle cell disease or sickle cell variants. Sickle cell patients may lose urine-concentrating ability for unknown reasons. This happens even with sickle cell variants but is less common.

    Chronic passive congestion. One cause of renal congestion is inferior vena cava obstruction. It produces mild diffuse tubular atrophy and hyperemia, leads to proteinuria (usually mild to moderate) and hyaline casts, and sometimes also elicits epithelial casts and a few RBCs. Occasionally, but not commonly, severe chronic passive congestion (CPC) may simulate the nephrotic syndrome to some extent, including desquamated epithelial cells containing fat plus many casts of the epithelial series. In CPC of strictly cardiac origin without significant previous renal damage, there is decreased urine volume but usually retained urine-concentrating ability. No anemia is present unless it is due to some other systemic etiology.

    Benign arteriosclerosis. Benign arteriosclerosis involves the renal parenchyma secondarily to decreased blood supply. In most cases in the earlier stages, there are few urinary findings, if any; later, there is often mild proteinuria (0.1-0.5 gm/24 hours) and a variable urine sediment, which may contain a few hyaline casts, epithelial cells, and perhaps occasional RBCs. If the condition eventually progresses to renal failure, there will be significant proteinuria and renal failure sediment with impaired renal function tests.

    Weil’s disease. Weil’s disease is leptospiral infection (Chapter 15) and clinically presents with hepatitis and hematuria. Characteristically, there are also high fever and severe muscle aching, and there may be associated symptoms of meningitis.

    Infectious mononucleosis. Renal involvement with hematuria occurs in 5%-6% of cases.

    Purpura and hemorrhagic diseases. These diseases should be recognized as causes of hematuria, either by itself or in association with glomerular lesions. The Henoch-Schцnlein syndrome (anaphylactoid purpura) is a rare condition featuring gastrointestinal bleeding (Henoch) or skin purpura (Sch?nlein) that often is concurrent with hematuria and nephritis.

    Hypersensitivities. Hypersensitivities may lead to proteinuria (usually slight) with hematuria and perhaps a moderate increase in casts. Kidney involvement may occur due to hypersensitivity to mercurials, sulfas, or other substances.

    Fat embolism. Fat embolism commonly occurs after trauma, especially fractures. Cerebral or respiratory symptoms develop the second or third day after injury, usually associated with a significant drop in hemoglobin values. Fat in the urine is found in about 50% of patients. Unfortunately, a physician’s order for a test for fat in the urine will usually result in microscopic examination of the sediment. Whereas this is the correct procedure to detect fat in the nephrotic syndrome, in which fat is located in renal epithelial cells and casts, it is worthless for a diagnosis of fat embolism, in which free fat droplets must be identified. Since free fat tends to float, a simple procedure is to fill an Erlenmeyer (thin-neck) flask with urine up into the thin neck, agitate gently to allow fat to reach the surface, skim the surface with a bacteriologic loop, place the loop contents on a slide, and stain with a fat stain such as Sudan IV.

    Hemochromatosis. This condition is suggested by hepatomegaly, gray skin pigmentation, and proteinuria in a diabetic patient. Proteinuria may exceed 1 gm/24 hours, but sediment may be scanty and fat is absent. In severe cases yellow-brown coarse granules of hemosiderin are seen in cells, in casts, and lying free. Prussian blue (iron) stains in this material are positive. Distal convoluted tubules are the areas primarily involved. Since hemochromatosis does not invariably involve the kidney until late, a negative urine result does not rule out the diagnosis. False positive results (other types of urine siderosis) may occur in pernicious anemia, hemolytic jaundice, and in patients who have received many transfusions.

    Thyroid dysfunction.

    Myxedema. Proteinuria is said to occur without other renal disease. Its incidence is uncertain, especially since some reports state that proteinuria is actually not common and usually persists after treatment.

    Hyperthyroidism. The kidney may lose its concentrating ability so that specific gravity may remain low even in dehydration; this is reversible with treatment and a return to a euthyroid condition. Occasionally, glucosuria occurs in patients.