We report a case of patient with documented SLE who displayed dysuria, gastrointestinal (GI) symptoms and renal insufficiency associated with the unusual occurrence of bilateral hydroureteronephrosis due to urterovesical junction stricture (obstructive uropathy). Pathologic investigations disclosed chronic interstitial cystitis (IC) with evidence of focal immune complex deposition in the blood vessel walls of the bladder. The GI symptoms and dysuria regressed with initial therapy for SLE with steroids. However, the persistent obstructive uropathy (OU) and renal insufficiency required bilateral nephrostomy followed by steroids plus intravenous pulse injection of cyclophosphamide. The obstructive uropathy was relieved even after removing the nephrostomy tube and renal function remained stable. Including this case, nineteen SLE patients associated with clinical and radiographic findings of OU were found in the world literature and reviewed to find any consistent pattern of clinical features. Most of the patients with OU in SLE were female (mean age, 31.7 yr) and orientals (63%), and had interstitial cystitis (89%) as a common underlying cause with concomitant involvement of the GI tract (89%) and WHO class IV or V advanced glomerulonephritis (67%). Despite the remarkable response (68%) to steroids in majority of OU patients associated with SLE, certain patients still required surgical correction (32%) and some even died (32%). OU, potentially reversible, was not an exception in patients with SLE, which might be overshadowed by other major organ involvement of SLE.

A rare case of bilateral renal cortical necrosis (BRCN) diagnosed only by the characteristic and specific findings of a contrast-enhanced CT scan during the acute initial phase of the disease is presented in this paper. Furthermore, twenty-eight patients of BRCN in the world literatures in English after 1980 were analyzed to investigate the changes in its clinical features over the past 15 years in comparison with the reported data before 1980 from two large centers in France (F) and India (I). Obstetric causes decreased from 68% (F) and 71% (I) before 1980 to 28% after 1980, whereas nonobstetric causes increased from 32% (F) and 29% (I) to 72% after 1980. Among the nonobstetric causes of BRCN, the leading causes were sepsis in 4 out of 12 patients (F) and snake bite in 6 out of 14 patients (I) before 1980, but, in contrast, drugs in 4 out of 21 patients after 1980. As a definite diagnostic procedure for BRCN, 95 to 100% before 1980 but 86% after 1980 performed renal biopsy, of which renal biopsy while living was done in only 42% (F) and 16% (I) before 1980 and 67% after 1980. None showed renal calcification in abdominal X-ray, and only 25% (3/12) had nonspecific echo findings in renal ultrasonography, whereas the high sensitivity for BRCN was noted in renal arteriography in 100% (6/6) and contrast-enhanced CT scan in 88% (7/8). The mortality of BRCN decreased from 55% (F) and 86% (I) before 1980 to 36% after 1980. This review of BRCN, in conclusion, revealed the distinctive changes over the past 15 years in the etiology with a higher incidence of non-obstetric causes than obstetric ones, diagnostic procedures with less dependence on renal biopsy but new trials of non-invasive radioimagings including CT scan and even MRI, and a further declining mortality rate.

Post-transplant lymphoproliferative disorders (PTLD) have been recognized as a complication of immunosuppression and occur with a reported incidence of 1 to 8% of recipients receiving solid organ transplantation. PTLD are classified into two major categories, polymorphic and monomorphic PTLD. The majority of the monomorphic PTLD cases are non-Hodgkin's lymphoma of B-cell origin. Hodgkin's disease is not part of the typical spectrum of PTLD; however, it has been rarely reported. We describe a case of Hodgkin's disease following renal transplantation. A 41-year-old man developed right cervical lymphadenopathy following renal transplantation 116 months previously for chronic renal failure of unknown origin. He had been taking cyclosporine, mycophenolate mofetil and prednisone. A lymph node biopsy revealed mixed cellularity Hodgkin's disease. Immunohistochemical staining was positive for CD30 and EBV-latent membrane protein-1. No other site of disease was identified. The immunosuppressive agents were reduced (mycophenolate mofetil was discontinued, cyclosporine dose reduced from 200 mg to 150 mg and prednisone continued at 5 mg). After 2 cycles of ABVD followed by radiation therapy (3600 cGy), he achieved complete remission.

The thromboembolic complications of nephrotic syndrome are reasonably common, including spontaneous peripheral venous and/or arterial, pulmonary arterial, and renal venous occlusions. However, in comparison to the relatively high incidence of the venous thromboembolic complications with hypercoagulable status, arterial thromboses have been reported much less and it was only 20 cases in the English literature so far. Furthermore, the most cases were pediatric patients rather than adults. Therefore, this report describes an adult nephrotic cases complicated by superior mesenteric artery thrombosis leading to death via catastrophic hospital course. Also, we reviewed the literature in English regarding cases of arterial thromboses in adult nephrotic patients with special interest to locations of thrombosis, underlying histopathologic types of glomerulopathy, and use of steroids or diuretics before its development.

Following the acute diarrhea in patients (n = 24) overnight with commonly used laxatives for bowel preparation, the changes in electrolytes and acid-base balance in blood and urine were investigated. Though no alterations of serum sodium or potassium concentrations were noted, mild but significant reduction of mean values (+/- SEM) of plasma pH and HCO3 after diarrhea when compared to those before it developed (pH, from 7.42 +/- 0.01 to 7.39 +/- 0.01, p < 0.01; HCO3, from 25.8 +/- 0.6 to 23.7 +/- 0.6 mEq/L, p < 0.05). However, significant reduction of concentration in spot urine sodium from 150 +/- 12.3 to 93 +/- 14 mEq/g of crea. (p < 0.01) and increase in spot urine potassium from 33 +/- 3.2 to 51 +/- 6.0 mEq/g of crea. (p < 0.05) following diarrhea were seen with significant reduction of urine pH from 6.67 +/- 0.21 to 5.5 +/- 0.13 (p < 0.001). Also, with this effective urinary acidification following diarrhea, a significant reduction of urinary anion gap as well as significant increment of spot urine ammonium was accompanied (anion gap, from 80.4 +/- 11.1 to 44 +/- 8.5 mEq/g of crea. p < 0.001; ammonium, from 87 +/- 18.5 to 229 +/- 37 mg/g of crea. p < 0.001) in addition to the significant inverse correlation between these changes in spot urine from basal levels in 24 study subjects (y = -1.13 x +61, r = 0.7, p < 0.001). In conclusion, we observed that the acute diarrhea with laxatives used for bowel preparation caused a mild degree of metabolic acidosis with no changes in blood electrolytes.(ABSTRACT TRUNCATED AT 250 WORDS)