Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.
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PMID:Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy. 910 53

The extensive use of selective histamine H2 receptor antagonists provides a unique opportunity to describe very rare adverse drug reactions. Although mild elevation of serum creatinine level following the administration of cimetidine is relatively common, acute interstitial nephritis (AIN) is a rare hypersensitivity reaction. There have been 25 published reports of AIN associated with H2 antagonist therapy and we also identified 16 cases from the Australian Adverse Drug Reaction Advisory Committee (ADRAC) database. AIN was reported most commonly following cimetidine administration. AIN was supported by renal biopsy in 28 patients and by rechallenge in 6. H2 antagonist-induced AIN was more commonly reported in men older than 50 years. In the majority of cases the onset was within 2 weeks of initiation of therapy (1 day to 11 months). The clinical manifestations were nonspecific including sterile pyuria, elevated erythrocyte sedimentation rate, fatigue, proteinuria and leucocytosis whereas rash, arthralgia and flank pain were rarely reported. There were 170 cases of hepatotoxicity following H2 antagonist administration reported to ADRAC. These were more common following ranitidine and included cholestatic, hepatocellular and mixed reactions. Hepatotoxicity was proven following liver biopsy in several cases published in the literature and in 15 cases reported to ADRAC. Hepatotoxicity recurred upon rechallenge in 6 cases. Generally, renal and hepatic adverse effects resolved quickly after cessation of H2 antagonist therapy and did not require specific treatment. Nephrotoxicity and hepatotoxicity following administration of an H2 antagonist is rare and a high index of suspicion is necessary for early detection. Now that many H2 antagonists are available over the counter, awareness of these conditions and early detection with cessation of H2 antagonist therapy would appear paramount.
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PMID:Nephrotoxicity and hepatotoxicity of histamine H2 receptor antagonists. 1121 86

A 27 year old patient presented with a sudden acute illness showing right flank pain, milky urine, nephrotic range proteinuria, erythrocyturia and leukocyturia in the urinary sediment with a negative leukocyte test stick. The proof of a pronounced hypertriglyceriduria led to the diagnosis of Chyluria. The lymphangiogram confirmed the presence of a retroperitoneal lymphatic dysplasia with evidence of communication with the right renal pelvis on the CT-lymphogram. Chyluria is generally the result of parasitic infection and is extremely rare in Europe. In the presence of symptoms including milky urine, proteinuria and leukocyturia in the urinary sediment and a negative urine leukocyte stick test and absence of infectious signs, chyluria must be suspected. The diagnosis should be substantiated through proof of hypertriglyceriduria and confirmed by lymphangiography.
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PMID:[A rare cause of nephrotic syndrome in a young woman with flank pain, milky urine and leukocyturia]. 1197 3

A 28-year-old female presented for evaluation of left flank pain and polyuria after having been exposed to cadmium in the jewelry manufacturing industry for approximately 3 years. This patient possessed both elevated 24-hr urinary ss2-microglobulin and elevated blood cadmium levels. Approximately 6 months after initial presentation, the patient resigned from her job due to shortness of breath, chest pain, and anxiety. Exposure to cadmium in the jewelry industry is a significant source of occupational cadmium exposure. Other occupational sources include the manufacture of nickel-cadmium batteries, metal plating, zinc and lead refining, smelting of cadmium and lead, and production of plastics. Cadmium is also an environmental pollutant that accumulates in leafy vegetables and plants, including tobacco. Major toxicities anticipated from cadmium exposure involve the renal, pulmonary, and, to a lesser extent, gastrointestinal systems. These include the development of renal proximal tubular dysfunction, glomerular damage with progressive renal disease, and respiratory symptoms including pneumonitis and emphysema. Low-level cadmium exposure has also been associated with increased urinary calcium excretion and direct bone toxicity, effects that recent research suggests may result in the development of osteoporosis. The body burden of cadmium, over half of which may reside in the kidneys, is most often measured through the use of urinary cadmium levels. Blood cadmium measurements generally reflect current or recent exposure and are especially useful in cases with a short exposure period and only minimal accumulation of cadmium in the kidneys. Both ss2-microglobulin and alpha1-microglobulin serve as organ-specific, early-effect biomarkers of tubular proteinuria and thus play a role in identifying early signs of cadmium-induced renal damage in those with potential exposures. In addition to ensuring workplace compliance with Occupational Safety and Health Administration-mandated monitoring and screening measures, it is prudent for those with cadmium exposure to maintain adequate intake of both iron and calcium, appropriate measures even in the absence of exposure.
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PMID:Cadmium exposure and nephropathy in a 28-year-old female metals worker. 1246 Aug 7

Venous thrombophilia is the result of clotting changes namely of a hypercoagulable state together with blood flow and vessel wall changes. There is no need for all these components to be present in order for thrombosis to occur. As the matter of fact, thrombosis may occur even if only one of these conditions is present. In clinical practice a combination of factors is usualy seen. In comparison with arterial thrombophilia, clotting changes and blood flow seen to play a major role in venous thrombosis. Venous thrombophilia may remain asynptomatic or may result in a series of clinical syndromes. The commonest of these are: 1. Superficial vein thrombosis, 2. Deep vein thrombosis of legs, 3. Deep vein thrombosis of arms, 4. Caval veins thrombosis, 5. Portal vein thrombosis, 6. Hepatic veins thrombosis, 7. Renal vein thrombosis, 8. Cerebral sinuses thrombosis, 9. Right heart thrombosis, 10. Miscellaneous (ovarian, adrenal veins thrombosis, etc.). Since the first two are widely and easily recognized, these is no need for an extensive discussion. Deep vein thromboses of upper limbs are not as frequent as those of lower limbs or of superficial phlebitis but they can still be recognized on clinical grounds and non invasive techniques. The remaining 7 syndromes are less common and therefore less frequently suspected and recognized. Of particular interest, among these less common manifestations of venous thrombophilia are hepatic vein and renal vein thrombosis. Hepatic veins thrombosis, sometimes part of inferior vena cava thrombosis is most frequently due to an isolated occlusion of hepatic veins thereby causing a form of venocclusive disease. Occasionally diagnosis may be difficult because of slow onset of symptoms (hepatomegaly, right flank pain, fever, ascites etc.). The same is true for renal vein thrombosis which may also be of difficult diagnosis since it causes proteinuria and flank pain. The proteinuria is often interpreted as due to a nephrotic syndrome which, incidentally, may cause by its turn renal vein thrombosis. Portal vein thrombosis and cerebral sinuses thrombosis on the contrary are more easily suspected because of ascites, adominal pain, jaundice or headache, eye proptosis, vomiting. Right heart thrombosis should be suspected in cases of recurrent pulmonary embolization. Ovarian or adrenal veins thrombosis are rare. The competent physician should always consider, given certain congenital or acquired conditions, the possibility to be facing a special form of venous thrombosis or a venous thrombosis in unusual sites. An early diagnosis, as often in medicine, is of paramount importance for a prompt treatment and a satisfactory outcome.
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PMID:Clinical aspects of venous thrombophilia. 1367 53

Although patients with systemic lupus erythematosus (SLE), especially those with antiphospholipid antibodies, have a high incidence of arterial and venous thrombotic manifestations, renal infarction has been rarely reported in these patients and is probably underestimated. A 9-year-old boy with renal infarction, diagnosed by computed tomography and scintigraphy, is described. Initially he complained of severe flank pain; he had no urinary abnormalities and his blood pressure was normal. No evidence of systemic disease was found. He responded well to antibiotic treatment without the need for immunosuppressive therapy. In subsequent years he presented a spectrum of clinical symptoms, including fever, malaise, arterial hypertension headache, and mononeuritis multiplex, accompanied by an increased erythrocyte sedimentation rate and transitory proteinuria. This suggested vasculitis involving peripheral vessels as well as the central nervous system. Treatment with oral prednisone and azathioprine led to remission. Four years after the renal infarction, the child presented with recurrence of systemic disease. The diagnosis of SLE was established, with positive antiphospholipid antibodies. The sudden appearance of severe unexplained flank pain should alert the clinician to a possible underlying renal vessel thrombosis. Renal venous thrombosis is probably much more common; however, renal arterial thrombosis and infarction in association with SLE with positive antiphospholipid antibodies should be added to the differential diagnosis.
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PMID:Renal infarction in a child with systemic lupus erythematosus. 1506 40

We present a patient with Fabry disease with remarkable diagnostic findings and gluten-sensitive enteropathy. An 11-year-old girl was admitted to hospital with weight loss, anorexia, nausea, vomiting, flank pain, acroparesthesia, and painful extremities. Her mother had end-stage renal failure secondary to Fabry disease. On physical examination, she had growth retardation. Ophthalmological examination showed characteristic whorl-like corneal opacities and Fabry disease was confirmed with low alpha-galactosidase A (alpha-gal A) activity. Her painful attacks were treated with carbamazepine, but vomiting and nausea continued. Laboratory studies revealed positive serum anti-endomysium and anti-gliadin antibodies. Small intestinal biopsy showed subtotal villous atrophy compatible with gluten-sensitive enteropathy. Following treatment with a gluten-free diet, her gastrointestinal symptoms completely disappeared within a few weeks and then she had catch-up growth. In her long-term follow-up, proteinuria appeared and renal involvement was confirmed by characteristic renal biopsy findings. Following these clinicopathological findings, enzyme replacement therapy was started. In conclusion, although heterozygous females can be asymptomatic or are expected to have a mild course of the disease, a severe clinical course in our patient in the 2nd decade is of particular interest. In addition, Fabry disease occurring with gluten-sensitive enteropathy, a very rare co-existence, is emphasized.
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PMID:The co-existence of Fabry and celiac diseases: a case report. 1508 21

Seven patients aged 13 to 17.5 years developed acute renal failure after treatment with a variety of non-steroidal anti-inflammatory drugs (NSAID): naproxen, diclofenac, ibuprofen, dipyrone and paracetamol. Six of the patients used more than one kind of NSAID. None of the patients had previous history of renal disease or concomitant treatment with other drugs. The time interval between NSAID administration to the emergence of symptoms ranged from 1 to 4 days. The most common presenting symptoms were flank pain (4 patients), abdominal pain (3 patients) and vomiting (3 patients). All patients had normal urine output. Microscopic hematuria and proteinuria were found in 5 patients and leukocyturia in 2. Serum creatinine ranged from 1.3 to 8.3 mg% at presentation. Kidney biopsy was performed in 3 patients and showed findings consistent with mild interstitial inflammation in 1 patient, and normal renal tissue in 2. All patients were treated with intravenous fluids, 1 received corticosteroids. Renal function completely normalized in all patients within 7 to 16 days.
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PMID:Acute renal failure, associated with non-steroidal anti-inflammatory drugs in healthy children. 1597 24

The nutcracker phenomenon refers to compression of the left renal vein between the aorta and the superior mesenteric artery. Clinical features are hematuria, abdominal pain, left flank pain, pelvic or scrotal discomfort due to varicocele or ovarian vein syndrome. In this report, 2 patients with orthostatic proteinuria, in whom nutcracker phenomenon was detected as a cause, are presented. One of them had posterior nutcracker with also asymptomatic varicocele that was detected during ultrasonographic examination. Nutcracker phenomenon is a rare but important clinical condition that should be considered in the differential diagnosis of patients with proteinuria and hematuria.
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PMID:The "nutcracker phenomenon" with orthostatic proteinuria: case reports. 1662 28

Compression of the left renal vein between the aorta and the superior mesenteric artery causes a physiological condition, the so-called nutcracker phenomenon, but it can sometimes lead to left venous hypertension, or "nutcracker syndrome". Classical manifestations of which are an association of left flank pain, unilateral proteinuria and unilateral hematuria, without renal impairment. We report an atypical association of nutcracker syndrome with IgM nephropathy.
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PMID:[Clinical case of the month. Nutcracker syndrome in association with a painful nephrologic disease]. 1746 Dec 94


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