Cases reported "Proteinuria"

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11/48. Acute interstitial nephritis predisposed a six-year-old girl to minimal change nephrotic syndrome.

    A six-year-old girl was admitted to our hospital with acute renal failure. We made a clinical diagnosis of acute interstitial nephritis and oral corticosteroid therapy was started. Her renal failure soon recovered, and renal biopsy showed acute interstitial nephritis by light microscopy with glomerular foot process effacement by electron microscopy. Although her proteinuria was not heavy at the time of biopsy, her proteinuria subsequently increased to show nephrotic syndrome. We continued to give corticosteroids and her nephrotic syndrome went into remission 13 days after biopsy. Serological and bacteriological examination showed no evidence of known pathogen or drug hypersensitivity. The time changes in proteinuria were monitored by fractional total protein excretion (FETP) and fractional beta2 microglobulin excretion (FEbeta2MG) in order to evaluate the severity of proteinuria under different glomerular filtration rates and different proximal tubular functions. The results revealed that nephrotic syndrome had occurred during recovery from acute interstitial nephritis. This is the first case report to show the sequential occurrence of acute interstitial nephritis and nephrotic syndrome based on evidence from fractional protein excretion.
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12/48. nephrotic syndrome and aberrant expression of laminin isoforms in glomerular basement membranes for an infant with Herlitz junctional epidermolysis bullosa.

    Herlitz junctional epidermolysis bullosa (H-JEB) is a hereditary bullous disease caused by absent expression of laminin-5, a component of anchoring filaments within the dermal-epidermal basement membrane zone. Affected individuals usually die during the first 1 year of life. We studied an infant with H-JEB who presented with nephrotic syndrome, a previously unreported complication that may contribute to early death in this disease. dna analysis revealed a compound heterozygote for mutations 2379delG and Q995X in the LAMB3 gene. The patient had massive albuminuria, attributable to failure of the glomerular filtration barrier, and high urinary N-acetylglucosaminidase levels, indicating renal tubular involvement. Electron-microscopic examination of the renal tissue revealed diffuse fusion of the foot processes, irregular swelling of the lamina rara interna, and disappearance of endothelial cell fenestrations. Immunohistopathologic analysis of the patient's renal tissue revealed compositional changes in laminin isoforms of the glomerular basement membrane and no detectable laminin-5 in the renal tubular basement membrane, which suggests that laminin-5 may play an important role in renal function. Our findings strongly suggest that H-JEB should be considered in the spectrum of congenital nephrotic syndromes. Combination therapy with meticulous skin care and treatment strategies established for congenital nephrotic syndromes may rescue patients with this disease.
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13/48. An adult with acute poststreptococcal glomerulonephritis complicated by hemolytic uremic syndrome and nephrotic syndrome.

    We report the case of a 47-year-old man with the simultaneous occurrence of clinical and laboratory features consistent with acute poststreptococcal glomerulonephritis (APSGN), hemolytic uremic syndrome (HUS), and nephrotic syndrome. Acute nephritic syndrome occurred 3 weeks after having pharyngeal pain and diarrhea. He presented with edema and hypertension on admission. Laboratory evaluation showed hemolytic anemia with fragmentation, thrombocytopenia, elevated lactic dehydrogenase level, low haptoglobin level, low complement c3 level, and elevated antistreptolysin-O titer. serum creatinine level was 1.22 mg/dL (108 micromol/L), and urinalysis showed marked proteinuria, with protein of 8.7 g/d, and hematuria. The renal biopsy specimen was characteristic of APSGN, but not HUS. Moderate expansion of the mesangial matrix, moderate proliferation of epithelial and endothelial cells, and marked infiltration of neutrophils was seen by means of light microscopy, and many subepithelial humps were seen by means of electron microscopy. Neither fibrin deposition nor evidence of thrombotic microangiopathy was found. complement c3 deposition along the capillary wall and tubules was seen in an immunofluorescence study. The patient was administered plasma infusion at 320 mL/d and antihypertensive drugs. serum complement c3 and haptoglobin levels returned to normal within 3 weeks. This is a rare case of the simultaneous occurrence of APSGN, HUS, and nephrotic syndrome.
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14/48. gastric bypass and resolution of proteinuria in an obese diabetic patient.

    There is few human studies evidence that suggest a role for obesity in the formation and progression of glomerular lesions. We report the case of a morbidly obese female with diabetic nephropathy that was subsequently diagnosed with renal failure. proteinuria resolved after gastric bypass procedure. The reduction of glomerular hyperfiltration and blood pressure associated with the important weight loss may be the major contributors to the decrease of proteinuria and serum creatinine levels in our patient.
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15/48. Post-MRSA infection glomerulonephritis with marked Staphylococcus aureus cell envelope antigen deposition in glomeruli.

    A 48-year-old male developed massive proteinuria and renal dysfunction after pneumonia caused by methicillin-resistant staphylococcus aureus (MRSA) infection. Examination of a renal biopsy specimen by light microscopy showed severe mesangiocapillary proliferative glomerulonephritis with fibrocellular crescents. Immunofluorescence microscopy showed weak linear staining for immunoglobulin g (IgG), while both the peripheral and mesangial lesions stained for IgA and C3. Immunostaining for a possible antigen related to post-MRSA infection glomerulonephritis, using monoclonal antibody S1D6, revealed marked deposition of S.aureus cell envelope antigen in the glomeruli. Electron-dense deposits were observed in both the subendothelial and the mesangial areas. Focal subendothelial widening accompanied with monocytes or foam cell infiltration was also seen. The findings reflect a typical post-MRSA infection glomerulonephritis caused by S.aureus cell envelope antigen.
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16/48. Complete remission of minimal-change nephrotic syndrome induced by apheresis monotherapy.

    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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17/48. Secondary focal segmental glomerulosclerosis following kidney transplantation in a patient with type I diabetes mellitus.

    Although recurrent diabetic nephropathy is common in patients with type I diabetes after kidney transplantation, the development of focal segmental glomerulosclerosis (FGS) is rare, and its development generally takes several years. We report here a case of type I diabetes mellitus with secondary FGS accompanied by proteinuria 10 months following kidney transplantation. Episode biopsy showed secondary FGS, evidenced by glomerular capillary collapse and large epithelial cells with ballooning degeneration. Exudative dense deposition of IgM in a diffuse global mesangial pattern and enlarged glomerular diameters were observed, suggestive of glomerular hyperfiltration which can lead to secondary FGS. An imbalance in body size between donor and recipient and/or uncontrolled diabetes are potential causes of glomerular hyperfiltration. We administered angiotensin-converting enzyme inhibitor and angiotensin ii receptor blocker to reduce hyperfiltration-induced renal damage; the combination therapy reduced proteinuria from 2346 to 258 mg/d. Secondary FGS should be a consideration after kidney transplantation in patients with type I diabetes mellitus.
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18/48. Reduction of proteinuria after gastric bypass surgery: Case presentation and management.

    obesity is increasing in prevalence across the united states. The surgical therapy for obesity is effective at reducing weight; however, the benefits to renal function are not well described. We report an obese patient with nonnephrotic-range proteinuria that resolved after Roux-en-Y gastric bypass. Evidence suggests that obesity-related renal dysfunction is multifactorial and may be a result of hyperfiltration or increased intra-abdominal pressure. The use of gastric bypass as a permanent solution to obesity may confer a similar benefit to obesity-related renal dysfunction.
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19/48. Nephropathy in IgG4-related systemic disease.

    Lymphoplasmacytic sclerosing pancreatitis ("autoimmune" pancreatitis) is the best-known manifestation of an unusual corticosteroid-sensitive systemic fibrosclerotic disease that is associated with high plasma immunoglobulin G4 (IgG4) and tissue infiltration with IgG4-secreting plasma cells. Pancreatic and biliary manifestations of this condition are well-reported, but reports of other systemic involvement are few. We report here a case of initially unrecognized autoimmune pancreatitis followed 5 years later by a focal sclerosing lymphoplasmacytic tubulointerstitial nephritis and concurrent membranous nephropathy. The patient presented with hypertension, a raised serum creatinine, proteinuria, elevated serum IgG4, and eosinophilia. Immunolabeling of renal tissue showed numerous IgG4 positive plasma cells with peritubular and glomerular subepithelial IgG4 deposition. On steroid therapy serum IgG4 levels normalized, the eosinophilia resolved, and there was improvement in symptomatic wheeze, dry eyes, serum creatinine, and liver function tests. This case highlights a distinctive and potentially treatable form of interstitial nephritis manifesting from a systemic immune disorder, and provides circumstantial evidence to support the notion that dysregulated IgG4 can precipitate the development of a form of membranous nephropathy.
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20/48. Corticosteroid- and furosemide-induced increase in proteinuria in nephrosis.

    A corticosteroid- and furosemide-induced excessive increase in proteinuria developed in a 34-year-old nephrotic patient with focal glomerulosclerosis. The concentration of urinary protein increased almost in parallel with that of urinary glucose. This finding indicates that corticosteroids and/or furosemide can promote the disturbance of the tubular reabsorption mechanism together with increases in glomerular permeability and glomerular filtration rate.
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