Gene/Protein Disease Symptom Drug Enzyme Compound
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Irregularities in motor response after continuing levodopa therapy of Parkinson disease (the "on-off effect") were assessed with the addition of L-alpha-methyldopa hydrazine (carbidopa) in a double-blind study. Thirteen of 20 patients improved while receiving carbidopa and levodopa while only four of 17 patients improved while receiving placebo and levodopa. Twenty-three of 37 patients improved in a subsequent non-blind trial of carbidopa plus levodopa. Improvement was not dependent on an increase in dose or frequency of levodopa administration. Adverse effects included dyskinesia, imbalance, and confusion; nausea was eliminated. On patient died of glomerulonephritis that predated the drug trial, but worsened progressively during and after it. Carbidopa's suppression of the "on-off effect" suggests that extracerbral factors may be important in this phenomenon.
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PMID:Treatment of "on-off effect" with a dopa decarboxylase inhibitor. 115 14

Twenty-six patients with hypertension secondary to acute poststreptococcal glomerulonephritis were treated by the rapid intravenous infusion of diazoxide. The average pretreatment systolic pressure was 159 mm Hg. Five minutes after administration, the average systolic pressure was 122 mm Hg (a 23% reduction). The average initial diastolic pressure was 104 mm Hg, which fell 5 minutes after diazoxide injection to 71 mm Hg (a 32% reduction). No hypotensive episodes were noted. Occasional episodes of nausea occurred. Concentrations of blood glucose increased after administration of diazoxide; however, no values were above 155 mg/dl. Diazoxide appears to be a safe antihypertensive drug that is effective in the treatment of hypertension secondary to acute poststreptococcal glomerulonephritis.
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PMID:Intravenous diazoxide in acute poststreptococcal glomerulonephritis. 118 52

We present two patients with Hantaan virus infection, admitted to the Department of Nephrology, Skopje, at the same time, with the same clinical presentation (chills, fever, abdominal pain, hemorrhages, nausea, headache, proteinuria, hematuria, oliguria, acute renal failure) but with different pathohistological findings and different disease courses. In the first case diffuse proliferative glomerulonephritis was found, with a complete recovery of renal function after a month, with a mild proteinuria and erythruria during the second and the third month. In the second case, glomeruli were normal in general, with slight mesangial proliferation found in two out of twenty, but interstitial edema, lymphocyte infiltrations and tubular changes were noted. Complete recovery was not noted after 3 months of follow-up. The patient is now without hemodialysis treatment, with polyuria, in the stable phase of chronic renal failure which is not improving.
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PMID:Different pathohistological presentations of acute renal involvement in Hantaan virus infection: report of two cases. 198 98

We studied the results of renal transplantation in 16 patients with renal amyloidosis and in 46 controls with primary glomerulonephritis. Amyloidosis was primary in five and secondary to familial Mediterranean fever (FMF) in 11. All patients received live related donor kidneys and the majority had one-haplotype HLA match. One- and 5-year graft and patient survival rates were comparable in both groups. Moreover, the frequency of acute rejection episodes and the mean serum creatinine values were not significantly different between members of the two groups. Significant gastrointestinal symptoms in the form of nausea, vomiting, abdominal pains, and diarrhoea occurred in seven of the patients with amyloidosis (43.7%) and in only one of the controls (2%) (P = 0.001). All seven recipients with amyloidosis who developed the gastrointestinal manifestations were receiving cyclosporin and six had FMF. Maintenance colchicine treatment prevented recurrence of FMF symptoms. In one patient discontinuation of colchicine was followed by recurrence of FMF symptoms. Recurrence of renal amyloidosis was not observed in five patients subjected to Trucut graft biopsies 1, 2, 3, 18 and 72 months post-transplantation. It is concluded that live-related donor kidney transplantation is a safe procedure in patients with amyloidosis and follows a course similar to glomerulonephritis patients.
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PMID:Study of live donor kidney transplantation outcome in recipients with renal amyloidosis. 797 Jan

Two cases of anti-neutrophil cytoplasmic antibody (ANCA)-associated necrotizing and crescentic glomerulonephritis are reported. A 12-year-old girl and a 10-year-old boy presented with polyarthritis, anaemia, haematuria, proteinuria, impaired renal function, anorexia, nausea, marked loss of weight and lethargy. The boy also had a vasculitic rash and anterior uveitis. Both children had diffuse cytoplasmic ANCA identified by indirect immunofluorescence and confirmed by specific enzyme-linked immunosorbent assay. Renal biopsies showed severe focal and segmental necrotizing glomerulonephritis with 100% crescents. They were treated with plasma exchange, prednisolone, cyclophosphamide and heparin. Within 1 month of commencing treatment, both had normal serum creatinine concentrations and ANCA was not detectable. Renal biopsies 6 weeks following commencement of treatment revealed quiescent disease, although up to 40% of glomeruli were sclerosed or had fibrous crescents. Following cessation of cyclophosphamide and heparin after 7 months and reduction in steroid dose, a biopsy at 10 months in the boy revealed quiescent disease, but the girl had recurrent disease associated with reappearance of a low titre of ANCA and small cellular crescents in 20% of the glomeruli. These cases reflect the potential usefulness of ANCA determination for categorizing paediatric patients, helping in the selection of therapy and as a possible marker of disease activity, similar to the experience in adults.
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PMID:Anti-neutrophil cytoplasmic antibody-associated glomerulonephritis in children. 843 72

A 56-year-old male with DM and HTN presented with flank pain and nausea. Review of systems was negative, physical examination was notable for mild hypovolemia and laboratory revealed BUN 51 mg/dl, creatinine (Cr) 5.1 mg/dl (baseline 1.5), Westergren ESR 122 mm/h, fractional excretion of sodium 0.2% and UA positive for blood and protein. Despite volume resuscitation the Cr continued to rise. Urine sediment analysis revealed granular casts, renal tubular epithelial cells and a negative Hansel's stain. Hemodialysis was initiated with Cr 13.7 mg/ dl for dyspnea and dysgeusia. Subsequent laboratory data revealed 2 separate positive anti-GBM antibody titers and prednisone therapy was initiated. Renal biopsy was performed for further diagnostic, therapeutic and prognostic information and demonstrated interstitial nephritis with linear IgG and albumin deposition consistent with diabetic nephropathy. Follow-up antibody titers were negative. prednisone was discontinued and Cr stabilized with conservative therapy. Anti-GBM antibody disease is characterized by circulating IgG antibodies directed against the glomerular basement membrane, specifically the alpha-3 (IV) collagen chain. Anti-GBM nephritis is a rapidly progressive, isolated glomerulonephritis in association with circulating anti-GBM antibodies. A positive immunofluorescence (IF) test is considered diagnostic in the appropriate clinical setting. Therapies include immunosuppressive agents to suppress new antibody production and plasmapheresis to eliminate circulating antibodies. Anti-GBM antibody is not rapidly cleared by steroid therapy and the recovery of renal function is rare if initiation Cr is greater than 7 mg/dl. This case demonstrates that the current ELISA for alpha-3 (IV) collagen is not pathognomonic for anti-GBM nephritis and that renal biopsy with IF for IgG and albumin may be indicated to prevent administration of potentially toxic treatment.
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PMID:Diabetic nephropathy with interstitial nephritis presenting with a false-positive anti-GBM antibody. 1203 99

We report the case of a young woman who had transient encephalopathy with nausea, cognitive impairment, 2 generalized seizures accompanied by visual impairment, and stenotic alterations of cerebral vessels lasting for weeks until complete resolution. These findings were associated with an elevated antideoxyribonuclease B level and biopsy-proven poststreptococcal glomerulonephritis. At the time of the encephalopathy, the patient had no electrolyte level disturbances, an only mildly elevated urea level, and moderate arterial hypertension and was on methylprednisolone therapy. For a couple of days, cranial magnetic resonance imaging showed multiple disseminated asymmetric hyperintensities on T(2)-weighted and fluid-attenuated inversion recovery, suggesting vasogenic edema. However, Doppler ultrasound examinations showed stenoses of extracerebral and multiple intracerebral arteries that persisted for several weeks, lasting considerably longer than the cerebral edema. This finding does not fit the context of hypertensive or steroid-induced encephalopathy, but is consistent with diagnosis of an accompanying vasculitis. Treatment with methylprednisolone for several weeks was associated with resolution of arterial stenoses and neurological symptoms, complete reversibility of Doppler sonographic findings, and significant improvement in renal function.
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PMID:Transient encephalopathy complicating poststreptococcal glomerulonephritis in an adult with diagnostic findings consistent with cerebral vasculitis. 1693 Dec 24

A 72-year-old woman was admitted to our hospital because of massive proteinuria of 2.2 g/day. She had seen a general practitioner for management of Basedow disease, diabetes mellitus and hypertension for 24 years. On admission, she complained of anorexia and nausea. Laboratory data showed serum creatinine of 3.62 mg/dL and MPO-ANCA of 68 EU. Renal biopsy revealed crescentic glomerulonephritis complicated with membranous nephropathy. Thiamazole (MMI), which was being given for Basedow disease for years, was withdrawn on the suspicion as a cause of MPO-ANCA. Three years after the withdrawal of MMI, renal failure slowly progressed to the end-stage, while MPO-ANCA was negative. She was introduced onto hemodialysis. At that time, MPO-ANCA became positive again, the titer being 12.9 EU. Therefore, we suspected a relapse of ANCA-related vasculitis and performed steroid pulse therapy on the patient with methylprednisolone at 0.5 g/day for 3 days. On hospital day 14, MPO-ANCA became negative. On day 25, however, severe acute pancreatitis developed and a pancreatic tumor lesion was found on CT. In spite of amelioration of the pancreatitis by medical treatment, the pancreatic tumor lesion did not show any significant change. On day 48, she died of multiple organ failure. Autopsy showed a mucinous cyst adenoma of pancreas and necrotizing pancreatitis. We suspected steroid therapy as the cause of the pancreatic lesions.
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PMID:[MPO-ANCA related vasculitis complicating mucinous cystadenoma of the pancreas and severe acute pancreatitis after steroid pulse therapy: a case report]. 1906 54

Renal involvement in leprosy has been reported rarely in the literature. Acute kidney injury in patients with leprosy is uncommon and may occur due to acute tubular necrosis, drug-induced interstitial nephritis and rarely crescentic glomerulonephritis. The latter with histologic confirmation of the diagnosis has been reported in very few cases of leprosy. A 25-year-old male, on therapy for multibacillary leprosy, was found to have deranged renal functions on evaluation for a history of nausea, vomiting, swelling and episode of haematuria. Kidney biopsy was performed twice over a period of 2 weeks, showing progression from diffuse proliferative glomerulonephritis to crescentic glomerulonephritis, pauci-immune in nature. The patient was treated aggressively with intravenous steroids, following which his renal functions stabilized. Crescentic glomerulonephritis, an extremely rare phenomenon in leprosy, should be considered in these patients presenting with features of acute kidney injury. Timely performed renal biopsy assists in accurate diagnosis and appropriate management of the patient, hence preserving renal parenchyma. Rapid progression from diffuse proliferative glomerulonephritis to crescentic glomerulonephritis in a patient with leprosy is described herein for the first time in the literature.
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PMID:Renal involvement in leprosy: report of progression from diffuse proliferative to crescentic glomerulonephritis. 2001 24

We report a previously unrecognized complication of severe acute kidney injury (AKI) after the administration of pegfilgrastim with biopsy findings of mesangioproliferative glomerulonephritis (GN) and tubular necrosis. A 51-year-old white female with a history of breast cancer presented to the hospital with nausea, vomiting and dark urine 2 weeks after her third cycle of cyclophosphamide and docetaxel along with pegfilgrastim. She was found to have AKI with a serum creatinine (Cr) level of 6.9 mg/dl (baseline 0.7). At that time, her AKI was believed to be related to prior sepsis and/or daptomycin exposure that had occurred 5 weeks earlier. She was dialyzed for 6 weeks, after which her kidney function recovered to near baseline, but her urinalysis (UA) still showed 3.5 g protein/day and dysmorphic hematuria. Repeat blood cultures and serological workup (complement levels, hepatitis panel, ANA, ANCA and anti-GBM) were negative. She received her next cycle of chemotherapy with the same drugs. Two weeks later, she developed recurrent AKI with a Cr level of 6.7 mg/dl. A kidney biopsy showed mesangioproliferative GN, along with tubular epithelial damage and a rare electron-dense glomerular deposit. Pegfilgrastim was suspected as the inciting agent after exclusion of other causes. Her Cr improved to 1.4 mg/dl over the next 3 weeks, this time without dialysis. She had the next 2 cycles of chemotherapy without pegfilgrastim, with no further episodes of AKI. A literature review revealed a few cases of a possible association of filgrastim with mild self-limited acute GN. In conclusion, pegfilgrastim may cause GN with severe AKI. Milder cases may be missed and therefore routine monitoring of renal function and UA is important.
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PMID:Relapsing acute kidney injury associated with pegfilgrastim. 2332 57


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