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Preeclampsia and superimposed preeclampsia usually develop after 20 weeks of gestation. We report a case of a 35-year-old Japanese woman who developed hypertensive disorders of pregnancy (HDP) before 20 weeks of gestation. She presented with hypertension and proteinuria at 9 and 11 weeks of gestation, respectively, and developed nephrotic syndrome at 17 weeks of gestation. She did not have definite hypertension or urinary abnormalities before pregnancy. The patient was serologically positive for the antinuclear antibody. However, the complement levels were normal and anti-phospholipid antibody was not detected. A renal biopsy performed at 18 weeks of gestation showed diffuse endotheliosis and tip lesions of secondary focal segmental glomerulosclerosis but no hypertensive changes of the arterioles. Although electron microscopic examination showed electron-dense deposits in the subendothelial lesions, they were considered nonspecific plasma exudation by mass spectrometry. An abortion was performed at 20 weeks gestation because the patient’s congestive symptoms due to nephrotic syndrome had worsened and marked fetal growth restriction was observed. After delivery, the patient’s symptoms resolved immediately without any additional treatment; however, continuous antihypertensive medication was required. Finally, the patient was diagnosed with HDP based on the renal biopsy findings and her clinical course after delivery. Compared to previous reports, this case describes the earliest onset of HDP. Thus, HDP should be considered as a differential diagnosis in pregnant women with hypertension or proteinuria presenting with symptoms before 20 weeks of gestation.

Cutaneous and systemic plasmacytosis (CSP) is a rare lymphoproliferative disorder that mainly affects middle-aged Asian individuals. Although Castleman disease is often complicated with various renal involvements, glomerulonephritis associated with CSP, which is considered as a variant of Castleman disease, is rare. This report presents the case of a 41-year-old Japanese man with nephrotic syndrome associated with CSP. Renal biopsy findings showed focal segmental glomerulosclerosis (FSGS) and diffusely mild segmental mesangial proliferation. Plasma cell infiltration in the interstitium was not observed. Electron microscopic findings showed diffuse foot process effacement, localized involvement of subendothelial space widening with amorphous materials, and endothelial cell swelling. Lymph node biopsy findings denied Castleman disease. His skin regions and proteinuria were successfully treated with prednisolone and cyclosporine. The causal relationship between CSP and FSGS is unknown. However, increased serum levels of IL-6 and VEGF and decreased VEGF expression in the podocyte may contribute to renal lesions in patients with CSP. To our best knowledge, this is the first case of a patient with FSGS associated with CSP.

Ureterosigmoidostomy is a urological intervention performed to treat various conditions such as invasive bladder cancer, bladder exstrophy, vesicovaginal fistula, or urethral trauma. However, this intervention may lead to several metabolic complications. Here, we report an interesting case with quadriparesis and intestinal paralysis resulting from severe hypokalemia (the serum potassium level, 1.8 mEq/L) and hyperchloremic metabolic acidosis [pH 6.927 and the arterial bicarbonate level, 8.0 mEq/L] in a 65-year-old man who had undergone bilateral ureterosigmoidostomy for bladder cancer 16 years earlier. The abdominal computed tomography scan also showed that massive fluid consisting of the mixture of the diverted urinary stream and feces was accumulated in the dilated distal colon. The treatment with intravenous potassium and sodium bicarbonate administration combined with the drainage of the diverted urinary stream from the distal colon resulted in the restoration of hypokalemia and acidosis followed by the improvement of quadriparesis and intestinal paralysis. The underlying mechanism and the treatment of metabolic complications after ureterosigmoidostomy are briefly discussed.

A 72-year-old woman exhibited elevated serum myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA) levels since 2006. Her serum creatinine (sCr) levels increased from 0.5 to 1.62 mg/dl in a stepwise pattern with proteinuria and hematuria up to January 2011. Renal biopsy indicated global sclerosis (14 %), fibrocellular crescents (28 %), and Swiss cheese-like appearance of the glomerular basement membrane (GBM) on light microscopy. IgG4 staining was negative. Immunofluorescent examination indicated granular staining with IgG and C3 along the GBM. MPO-ANCA-associated glomerulonephritis with membranous nephropathy (MN) was diagnosed. As chronic changes were relatively evident in the renal biopsy specimen without acute augmentation of renal function, immunosuppressive therapy was not administered. Thereafter, rapidly progressive renal dysfunction occurred (sCr, 3.67 mg/dl in May 2011) with proteinuria (~2 g/day), hematuria, and elevated serum MPO-ANCA levels. Therefore, a second renal biopsy was performed in May 2011, indicating global sclerosis (42 %) and cellular crescents (35 %) on light microscopy. Electron microscopy indicated electron-dense deposits in the GBM and mesangial lesions. Steroid therapy was subsequently initiated, and the patient's renal function partially improved. MPO-ANCA levels decreased to within normal limits and hematuria disappeared. MPO-ANCA-associated glomerulonephritis with MN is a rare dual glomerulopathy. However, complication should be considered when urinary protein appears in large amounts. Secondary MN was suspected due to the lack of IgG4 staining and distribution of electron-dense deposits to the mesangial lesion. Renal dysfunction occurring in a stepwise pattern may be attributed to intermittent augmentation in MPO-ANCA-associated glomerulonephritis.