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)

We report a case of a 17-year-old male with relapse of minimal-change nephrotic syndrome (MCNS), in whom apheresis monotherapy without steroids or immunosuppressants resulted in complete remission. The patient initially developed nephrotic syndrome in February 1998. The first renal biopsy confirmed the diagnosis of MCNS. The patient was also found to be a carrier of hepatitis B virus. Steroid therapy was started with oral prednisolone 60 mg/day. Complete remission was achieved in 3 months, and the steroid treatment was tapered off in May 2001. During the steroid tapering, temporal exacerbation of liver function was noted. In July 2002, the patient was admitted to our hospital again due to relapse of nephrotic syndrome. Second biopsy reconfirmed the diagnosis of MCNS. Since the serum titer of HBV was elevated, apheresis monotherapy was selected to avoid the risk of steroid-induced fulminant hepatitis. Four sessions of low-density lipoprotein apheresis (LDL-A) and 5 sessions of double-filtration plasmapheresis (DFPP) reduced the proteinuria from 9.2 g/day to 0.2 g/day over 38 days without any additional medication. Proteinuria remained suppressed below 0.2 g/day for more than 12 months and no exacerbation of liver function was observed up to the final follow-up in September 2003. The present case suggested the potential of apheresis monotherapy to induce and maintain complete remission of MCNS and an important role of circulating factors in the pathogenesis of MCNS.
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PMID:Complete remission of minimal-change nephrotic syndrome induced by apheresis monotherapy. 1679 38

C1q nephropathy (C1qNP) is a controversial and uncommon form of glomerulonephritis, characterized by mesangial immunoglobulin and complement deposits, predominantly C1q, with no evidence of systemic lupus erythematosus. Clinically, it may present as nephrotic syndrome and non-nephrotic proteinuria per se or associated with microhematuria, hypertension, or renal insufficiency. We describe two sisters with C1qNP, who presented with steroid-resistant nephrotic syndrome. Both sisters presented before the age of 2 years, and they showed a poor response to other immunosuppressive therapy. Both girls had normal serum complement levels, negative antinuclear antibodies (ANAs) and negative hepatitis B antigen. Renal biopsy in both patients showed histological features of mesangioproliferative glomerulonephritis, with diffuse "full-house" positive immunofluorescence reaction in the mesangial area. The immunofluorescence reaction for C1q was most intense and co-dominant with IgG in both patients. Correspondingly, electron microscopy demonstrated dense deposits mainly in the mesangial areas too. We report on two young sisters with the characteristic features of C1qNP presented in early childhood. To the best of our knowledge, this is the first report of C1qNP in siblings.
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PMID:C1q nephropathy in two young sisters. 1795 93

We present the case of a 22-year-old male with chronic hepatitis B virus (HBV) infection, who developed nephrotic syndrome and had complete remission after lamivudine monotherapy. Renal biopsy showed membranous glomerulopathy, and the serum titer of HBV DNA increased to 1,130,000 copies/mL. As symptomatic therapy with angiotensin converting enzyme inhibitors did not improve the nephrotic syndrome, lamivudine 100 mg per day was started. His alanine aminotransferase level normalized 2 months after treatment, then hepatitis B e antigen seroconversion developed and serum HBV DNA became undetectable. His proteinuria improved subsequently and his leg edema disappeared completely 6 months after treatment. Neither hepatitis nor nephrotic syndrome had relapsed by month 13 when he came for follow-up. This suggests that lamivudine monotherapy may induce and maintain complete remission of membranous glomerulopathy associated with hepatitis B.
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PMID:Complete remission of nephrotic syndrome of hepatitis B virus-associated membranous glomerulopathy after lamivudine monotherapy. 1796 68

In a 56-year-old white male patient, a membranoproliferative glomerulonephritis Type I was diagnosed after a 12-month history of low grade B cell lymphoma (Binet A). HIV, Hepatitis B and C serology were negative. Due to an impairment of renal function despite chemotherapy with COP, an immunochemotherapy consisting of rituximab (6 cycles) and bendamustine (4 cycles) was given. This therapeutic approach caused a complete remission of the nephrotic syndrome. Renal function and arterial hypertension improved markedly. In addition, urinary sediment became normal and proteinuria disappeared completely.
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PMID:Remission of a B cell CLL-associated membranoproliferative glomerulonephritis Type I with rituximab and bendamustine. 1839 3

Clq nephropathy (Clq N) is an infrequent disease and only about 100 cases have been reported. It is defined by a pattern of immunofluorescence (IF) with dominant or co-dominant complement Clq with electron-dense deposits in the mesangium, without clinical or serological features of Lupus Nephritis. The most common histopathological findings of ClqN are focal segmental glomerulosclerosis and Minimal Change Disease. We report a 17 year-old male patient with an isolated selective proteinuria found in a routine study. He had normal renal function and urine culture was negative. Serum lipids, liver enzymes an complement were all normal. Serum antinuclear and anti-DNA antibodies, antineutrophil cytoplasmic antibodies (ANCA), HIV, Hepatitis B and C serology, were negative. Renal and abdominal ultrasonography was normal. The histopathological study revealed segmental glomerular sclerosis, moderate increase of mesangial matrix, Bowmann capsule adhesions and fucsinophil deposits in mesangium. The IF was positive (dominant) for Clq (+++) and IgA, IgG, IgM, C3++, all of them with a granular mesangial distribution. Ultrastructural findings were pedicelar effacement and paramesangial electron-dense deposits. Tubular reticular inclusions (TRI) were not found. Remission of proteinuria was reached after 18 months of treatment with enalapril and losartan. The patient remains with normal renal function. Clinical findings, negative serology for Lupus, light microscopy IF with dominant positivity for Clq, absence of TRI and paramesangial electron-dense deposits in electron microscopy lead us to the diagnosis of ClqN. A poor response to steroid therapy was described in ClqN. Thus it was worthwhile to differentiate it from lupus nephritis, that is responsive to steroids.
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PMID:[C1q nephropathy. Report of one case]. 1919 28

Steroid resistant nephrotic syndrome (SRNS) remains a challenge facing pediatric nephrologists. The underlying histopathology usually affects the course of the disease and the response to treatment. We studied the pattern of histopathology in children with SRNS who presented to the King Abdul Aziz University Hospital (KAUH), Jeddah, Saudi Arabia. The records of all children with primary SRNS, who were seen between 2002 and 2007 were reviewed. Only patients who had undergone a renal biopsy were included in the study. The histopathology slides were reviewed by two renal pathologists independently. Patients with congenital nephrotic syndrome, lupus or sickle cell disease, were excluded from the study. Thirty-six children fulfilled the inclusion criteria, and included 25 girls and 11 boys with female to male ratio of 2.3:1. Fifty percent of the children (n=18) were Saudi and the remaining 50% were from various other racial backgrounds (9 Asians, 4 Arabs, 2 Africans and 3 from the Far East). Their mean age at presentation was 4.3 +/- 3.0 years (range 1-12 years). The mean serum albumin at presentation was 15.6 +/- 7.1 g/L and all of them had 4+ proteinuria on urinalysis. Five children had elevated serum creatinine at presentation while the mean serum creatinine was 50.4 +/- 45.6 micromol/L. Three children had low serum complement levels at presentation and none were positive for hepatitis B surface antigen or antinuclear antibody (ANA). The renal histopathology was compatible with focal and segmental glomerulosclerosis (FSGS) in 39% (n=14), IgM nephro-pathy in 28% (n=10), mesengioproliferative glomerulonephritis (MesPGN) in 17% (n=6), mini-mal change disease (MCD) and C1q nephropathy (C1qNP) in 8% each (n=3 + 3) and IgA nephro-pathy in 3% (n=1). Our retrospective review shows that FSGS was the commonest underlying histopathology in children who presented with SRNS followed by IgM nephropathy and other variants of MCD such as MesPGN. C1qNP was the underlying cause in some children.
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PMID:Pattern of steroid resistant nephrotic syndrome in children living in the kingdom of Saudi Arabia: a single center study. 1973 91

We herein present a case of membranous nephropathy associated with chronic hepatitis B following acute hepatitis B virus (HBV) infection. A 22-year-old man was admitted to our hospital for evaluation of proteinuria, pitting edema on both legs, and increased body weight in December 2002. At the age of 18, he had suffered from acute hepatitis A and syphilis, and was found to be negative for hepatitis B surface antigen (HBsAg). Furthermore, he suffered from acute hepatitis B (AH-B) at the age of 21; he was found to be positive for HBsAg and anti-IgM antibody to core antigen (IgM HBcAb). However, he discontinued outpatient treatment before confirmation of HBsAg clearance or the appearance of antibody to HBsAg (HBsAb). At the present admission, HBsAg, antibody to hepatitis B e antigen (HBeAg), and HBcAb were positive, while IgM HBcAb was negative. His genotype of HBV was type A (HBV/A). Histopathological findings of the renal biopsy specimen confirmed glomerulonephritis and glomerular deposition of HBsAg. Thus, he was diagnosed as having nephrotic syndrome caused by membranous nephropathy (MN) associated with chronic hepatitis B (CH-B) following AH-B. Although interferon-alpha (IFN-alpha) administration was started for the treatment and temporary improvement of proteinuria was observed, remission of MN was not achieved.
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PMID:Membranous nephropathy associated with chronic hepatitis B occurring in a short period after acute hepatitis B virus infection. 2019 Apr 69

Although most cases of immunoglobulin A (IgA) nephropathy are idiopathic, several diseases are associated with IgA nephropathy. Of these, chronic liver disease resulting from hepatitis B or C virus infection has been reported as a secondary cause of IgA nephropathy. Recently, hepatitis A virus (HAV)-associated kidney disease has received attention because acute kidney injury can occur as a complication of HAV infection, generally caused by acute tubular necrosis or interstitial nephritis. However, unlike IgA nephropathy related to hepatitis B or C, HAV-associated IgA nephropathy is extremely rare and long-term outcomes have not been reported yet. We describe a case of spontaneous remission of IgA nephropathy associated with serologically documented HAV infection. The patient presented with microhematuria and moderate proteinuria, but acute kidney injury did not occur during active hepatic injury. Kidney biopsy specimens clearly showed mesangial IgA deposits with intact tubules and interstitium. Serum liver enzyme levels returned to reference values 1 month after the onset of acute hepatitis, but urinary protein excretion remained increased. Approximately 1 year later, urinary abnormalities were resolved and a second biopsy showed no mesangial IgA deposits. These findings suggest that IgA nephropathy can transiently accompany HAV infection, but may not progress to chronic glomerulonephritis after recovery from HAV.
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PMID:Spontaneous remission of IgA nephropathy associated with resolution of hepatitis A. 2093 22

Renal disease is not uncommon in those infected with HIV. The most common manifestation of HIV in the kidney is HIV-associated nephropathy (HIVAN). Other HIV- and non-HIV-related causes have been described in the literature. Immunotactoid glomerulonephritis (ITG) is a rare disorder found in 0.06% of renal biopsies characterized by organized tubular immune complex deposits, observed more often in Caucasians. ITG tends to occur in an older age group and in some patients has been associated with a hemopoietic malignancy. In this report, we describe a case of ITG occurring in an HIV-positive, hepatitis C (HCV)- and hepatitis B (HBV)-negative female, who presented with microscopic hematuria and proteinuria. A percutaneous kidney biopsy showed diffuse membranous glomerulopathy, with mild mesangial proliferation and segmental sclerosing lesions containing mainly IgG, Kappa- and C3-positive deposits. Electron microscopy revealed diffuse subepithelial tubular deposits diagnostic of ITG. Out of 5 reported HIV-positive cases and ITG in the literature, 3 were HCV+, 2 were Caucasian and 3 were African-American (AA) without detectable hematologic malignancy. We report another case of ITG in an HCV- and HBV-negative, AA female.
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PMID:An uncommon glomerular disease in an HIV patient: value of renal biopsy and review of the literature. 2117 55

Epidemiological studies have shown a relationship between hepatitis B virus (HBV) infection and development of proteinuria in some patients (most commonly children), with a predominance for male gender and histological findings of membranous nephropathy on renal biopsy. The presence of immune complexes in the kidney suggests an immune complex basis for the disease, but a direct relation between HBV and membranous nephropathy (or other types of glomerular diseases) remains to be proven. Clearance of HBV antigens, either spontaneous or following antiviral treatments results in improvement in proteinuria. Thus, prompt recognition and specific antiviral treatment are critical in managing patients with HBV and renal involvement. The present review focuses on treatment of HBV with special emphasis given to antiviral therapies, its complications, and dosing in patients with HBV-associated kidney disease.
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PMID:Treatment of hepatitis B virus-associated nephropathy. 2167 38


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