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 37-year-old man with multiple nodules on a chest X-ray film, hypertension, and proteinuria was admitted to our hospital in September, 1993. Thirteen years earlier, he had been admitted to another hospital because of bloody sputum, fever, and dyspnea. He also had slight oral aphthae and slight iridocyclitis. A chest X-ray film at that time showed bilateral diffuse reticular shadows, and his illness was diagnosed as acute interstitial pneumonitis. Since that time, he had been continuously receiving tapering doses of prednisolone. His chest symptoms were relieved, and the findings on the chest X-ray film resolved with that treatment. In 1993, he also had positive tests for HBs antigen and for HLA-B51, and he was found to have renal vascular hypertension. Chest CT films and a pulmonary angiogram showed multiple aneurysms and occlusions of pulmonary arteries. A renal angiogram showed multiple intraparenchymal aneurysms of renal arteries. A specimen taken by open-lung biopsy showed healed endoarteritis obliterans of muscular arteries and no alveolitis. His illness was diagnosed as polyangiitis overlap syndrome, because of the unclassified systemic necrotizing vasculitis.
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PMID:[Polyangiitis overlap syndrome with multiple pulmonary aneurysms and renal vascular hypertension]. 869 63

Mitochondrial encephalomyopathy is a hereditary syndrome showing impairment of muscle and the central nervous system. In this disorder, the following three syndromes have been identified on the basis of characteristic symptoms: Kearns-Sayre syndrome (KSS), mitochondrial encephalomyopathy with lactic acidosis, and stroke-like episodes (MELAS), and myotonic epilepsy with ragged-red fibers (MERRF). In this report, we describe a case of mitochondrial encephalomyopathy with renal disease. A 25-year-old man was referred to our hospital in May, 1992 for evaluation of long-standing proteinuria. He had a small stature, exotropia and no pretibial edema. No mental retardation was observed. Urinary protein excretion was 2.0 g/day and urine sugar was negative. Laboratory examination revealed a serum urea nitrogen 19 mg/dl, and a creatinine value of 1.5 mg/dl. Creatinine clearance was 45.8 ml/min. His serum and spinal fluid lactate value were elevated. Biopsied muscle showed an absence of ragged-red fibers, and the presence of an A-to-G point mutation at nucleotide pari 3243 in the mitochondrial tRNA(Leu(UUR)) in peripheral blood leucocytes. He was thought to have MELAS. On the renal biopsy specimens, light microscopic examinations showed minor glomerular abnormalities with two glomerular collapses and tubulo-interstitial damage. Electron microscopic examinations showed partial thickening of the glomerular basement membrane. We report here this rare case of MELAS with renal disease, and also review seventeen cases of mitochondrial encephalopathy associated with renal disease. The existence of a relationship between mitochondrial disorder and renal damage remains obscure.
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PMID:[A case of mitochondrial encephalomyopathy (MELAS)]. 871 14

We report the first case of the use of ibuprofen for the management of steroid-resistant nephrotic syndrome. A 41 year-old man with nephrotic syndrome, secondary to focal segmental glomerulosclerosis, had persistent nephrotic range proteinuria despite aggressive treatment with steroids and cyclophosphamide. His steroid-resistant nephrotic syndrome resolved rapidly when he was serendipituously started on ibuprofen for the treatment of pericarditis. His proteinuria remained low at about 0.5 g/day over the next two years of treatment with ibuprofen and without any increase in his serum creatinine. He did not receive any ACE inhibitor or calcium channel blocker. An attempt to discontinue ibuprofen resulted in the relapse of his nephrotic syndrome. Upon restarting ibuprofen, his proteinuria decreased to less than 0.5 g/day again. We conclude that ibuprofen has been effective and safe for the management of nephrotic syndrome in this patient. However, careful monitoring is prudent to assess the potential adverse effects of ibuprofen on renal function with prolonged use.
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PMID:Successful management of steroid-resistant nephrotic syndrome using ibuprofen. 902 Dec 45

A 19-year old caucasian patient suffered from ulceration and scaring of his fingers since age two. During childhood, fibrosing contractures on the phalanges developed. Since puberty, his eunuch-like stature, bird-like face and exophthalmos had become under obvious. His hair was extraordinarily fine; his pubic hair rare. Radiological examination revealed ankylosis and osteoporosis of the phalanges and carpals. Angiography showed occlusion of multiple digital and interdigital arteries. Furthermore, a bilateral posterior cataract, restrictive respiratory disease, impaired glucose tolerance, hyperuricemia, proteinuria and primary hypogonadism were diagnosed. These findings are characteristic for the premature aging syndromes. The cardial symptoms of tall stature, bird-like face, pseudoexophthalmos, skleroderma-like and poikiloderma-like cutaneous lesions, scarce hair growth, early diabetes mellitus and arteriosclerosis led to the diagnosis of metageria.
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PMID:[Metageria--clinical manifestations of a premature aging syndrome]. 941 Aug 52

Nine days after working in the woods, a previously healthy 32-year-old man fell seriously ill. His symptoms included high fever, chills, diffuse myalgia, severe headache, and back pain. On the fifth day of onset of symptoms, blood tests showed creatinine levels of 5.4 mg/dL accompanied by marked proteinuria. After admission to the hospital, a diagnosis of nephropathia epidemica (NE) caused by Puumala virus was made using solid-phase enzyme-linked immunosorbent assay (ELISA). The patient gradually recovered renal function without requiring dialysis. However, he surprisingly experienced a sharp decline in platelet count to a minimum of 2,000/microL with concomitant occurrence of petechiae and conjunctival hemorrhage. Prednisolone was initiated, resulting in a swift rise in platelets. Six days later, when the medication was withdrawn, a sharp decrease in platelets recurred. The steroids were then readministered for the next 3 months, thus reestablishing a stable platelet count. The immediate rise of platelets after administration of prednisolone supports the pathophysiological view of hantavirus infection as an immunologically mediated disease. Corticosteroids in the treatment of hantavirus-associated thrombocytopenia might need further systematic evaluation.
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PMID:Severe thrombocytopenia and response to corticosteroids in a case of nephropathia epidemica. 942 61

Although systemic AA amyloidosis complicating Crohn's disease has been found in 0.5 to 6% in America and Europe, it is relatively rare in Japan. We report a case of systemic AA amyloidosis complicating Crohn's disease. In 1979, a 26-year-old Japanese man presented with diarrhea, melena and perianal abscesses, and was diagnosed as having Crohn's disease. He was treated with oral prednisolone, salazosulfapyridine and diet therapy. However, the gastrointestinal symptoms recurred and he was hospitalized several times. In 1991, his thyroid gland was found to be swollen, but with normal thyroid function, and his thyroid gland became larger subsequently. In October 1995, he showed renal dysfunction (blood urea nitrogen 33.2 mg/dl; serum creatinine 1.5 mg/dl) with proteinuria. His renal function had been deteriorating rapidly. On September 13, 1996, he was admitted to the Tsukuba University Hospital. At the time of admission, his renal function showed a blood urea nitrogen of 129.5 mg/dl with a creatinine of 5.4 mg/dl. The urine contained 0.8 g of protein per 24 hours. He presented with diarrhea for several days before admission and was treated with central venous hyperalimentation. Despite supportive care, he developed end-stage renal failure, then hemodialysis was initiated on October 7. His condition was complicated by a complete auriculoventricular block on October 18. He died of hemoperitoneum on October 25. On postmortem examination, extensive amyloid deposits were found in multiple organs including kidneys, intestine, heart, thyroid gland, lungs, liver, spleen, pancreas, gall bladder, adrenal glands, testis, prostate, bone marrow and parathyroid glands. Analysis of amyloid protein in the autopsy specimens showed type AA.
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PMID:[A case of systemic AA amyloidosis complicating Crohn's disease]. 965 12

We report a case of a 37-year-old man with relapsing polychondritis and IgA nephropathy. He visited our hospital with high fever and the swelling of his ears and eyelids. His symptoms and the results of the biopsy of his right auricle fulfilled the Damiani's criteria. Laboratory examination on admission showed an increase of serum IgA level, a presence of immune complex, remarkable hematuria (grade III) and proteinuria (grade II). Most of his symptoms were improved by the administration of antibiotic and NSAIDs, however, urinary findings still remained unchanged. The biopsy of his right kidney led to a diagnosis of IgA nephropathy (group II). Although relapsing polychondritis is known to associate rarely with renal involvement, it is very rare to associate with IgA nephropathy. This case indicates that immune disorders including IgA nephropathy should be investigated in patients with relapsing polychondritis.
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PMID:[A case of relapsing polychondritis with IgA nephropathy]. 988 50

A family (a brother and a sister) of the familidal isolated hyperparathyroidism (FIH) was reported. The older brother with age of 58 year-old was pointed out hypercalcemic while examining his hypertension and proteinuria. He had high levels of serum total and ionized calcium, intact-PTH and gastrin, and hypophosphatemia. His neck CT scan revealed swelling of the two parathyroid glands in each side. He underwent resection of the tumors and the auto-implantation of the glands under diagnosis of primary hyper parathyroidism. Histopathology was diagnosed to be hyperplasia of the parathyroid glands. The younger sister with age of 52 year-old was referred to our clinic because she was suffering from recurrent urolithiasis. Biochemical examination of her blood sampling resulted in very resemble values of her brother mentioned above. Her neck CT scan showed three tumors consisting of each one at the bilateral parathyroid glands and one in the thymic region. She underwent resection of the tumors and the auto-implantation of the glands and histopathological diagnosis was hyperplasia as same as her brother's one. The postoperative courses of these cases have been uneventful for four years. FIH is a low significant disease of which ten lineages have been reported in Japanese literature although it should be differentiate with such a disease of multiple endocrine neoplasms.
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PMID:[Familial isolated hyperparathyroidism: a report of two cases]. 1068 81

Previous reports have clarified that focal and segmental glomerulosclerosis(FSGS) appearing in membranous nephropathy(MN) is associated with a poorer prognosis than that of MN without FSGS. However, the etiology and pathogenesis of such FSGS lesions may show substantial individual differences. In some patients, hemodynamic alterations secondary to hypertension and vascular disorders seem to play a crucial role in the development of such FSGS lesions. In such instances, steady regulation of blood pressure might slow down further progression of FSGS lesions. Here we describe two cases of biopsy-proven MN with FSGS. Case I was a 44-year-old man who had shown massive proteinuria with hematuria at the age of 39 years. Renal biopsy specimens obtained at the age of 40 and 41 years showed MN without FSGS and MN with FSGS, respectively. His blood pressure control was fairly good throughout the course. Although he was on a steroid, an immunosuppressant, a low protein diet, and an ACE inhibitor, his renal function declined in 5 years. Case 2 was a 61-year-old woman who showed nephrotic syndrome at the age of 39 years. A renal biopsy specimen obtained at the age of 58 years showed MN with FSGS and remarkable atherosclerotic changes of the interlobular arteries. Her blood pressure control was rather poor throughout the course. Her renal function gradually declined over 22 years. Since parts of the FSGS lesions of the second case may have been caused by hypertension, it is tempting to speculate that day-to-day control of blood pressure could improve the long-term prognosis. We believe that, at least in some patients of MN with FSGS, careful management may lead to a more favorable course of decline in renal function.
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PMID:[Two cases of idiopathic membranous nephropathy with focal and segmental glomerulosclerotic lesions in which renal function progressively deteriorated]. 1099 19

We report a patient, a 23-year-old man, who was a hepatitis B virus(HBV) carrier complicated with nephrotic syndrome. He was admitted to our hospital because of generalized edema and massive ascites. Laboratory data on admission were as follows: proteinuria 9,850 mg/day, Cr 2.7 mg/dl, BUN 73 mg/dl, albumin 1.9 g/dl, cholesterol 501 mg/dl, GOT 23 IU/l, GPT 19 IU/l, HBsAg(+), and HBeAg(222.7). Since his nephrotic symptoms were seriously complicated with renal failure, we selected steroid therapy for nephrosis preference. His renal function was improved and the urinary protein decreased immediately, but his liver function deteriorated. The renal biopsy revealed focal mesangial proliferative glomerulonephritis. Immunofluorescent examination revealed slight deposits of IgG, IgM, and C3 along the glomerular basement membrane and mesangial matrix. He was not compliant and often stopped taking the steroid therapy, thereby causing nephrosis to recur each time. After all, nephrotic symptoms have been well-controlled with cyclosporin and steroid. In spite of the seroconversion of HB virus by formation of HBe antibody, mutant HBV infection continued. The fact that liver biopsy revealed severe lymphoid infiltration at the portal area suggested chronic active hepatitis. His clinicopathologic course suggests that HBV-associated nephropathy does not always remit as there are some cases in whom hepatitis remains in an active state even after seroconversion, due to its mutant status. In these cases, the long-term prognosis of HBV nephropathy has not been defined. Further study is necessary to establish the optimal treatment for HB nephropathy in adults.
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PMID:[A case of hepatitis B virus carrier complicated with nephrotic syndrome]. 1099 20


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