Lovastatin in glomerulonephritis patients with hyperlipidaemia and heavy proteinuria.

Lovastatin, a 3-hydroxy-3-methylglutaryl coenzyme A inhibitor, was given to 14 patients with unremittent nephrotic syndrome (heavy proteinuria with hyperlipidaemia) for 6 months. Treatment was started at an initial dose of 20 mg/day, increasing to a maximum of 80 mg/day. Treatment was well tolerated except in two patients: one developed rhabdomyolysis and one severe hypertriglyceridaemia requiring an additional antihyperlipidaemic agent. Lovastatin was effective in reducing serum cholesterol, LDL-C and apolipoprotein B in the remaining 12 patients. Cholesterol was reduced by 31% from 8.24 +/- 0.49 mmol/l (mean +/- SEM) to 5.7 +/- 0.18 mmol/l after 6 months (P less than 0.001). LDL-C was normalized to 3.26 +/- 0.21 mmol/l from a pretreatment value of 5.76 +/- 0.48 mmol/l (P less than 0.001), a decrease of 43%. Serum apolipoprotein B was also normalized to 1.11 +/- 0.09 g/l from a basal level of 1.51 +/- 0.10 g/l (P less than 0.05). Triglyceride, HDL-C and apolipoprotein A1 concentrations were unchanged. Proteinuria as well as renal albumin clearance were unchanged. GFR by plasma radioisotope Cr-EDTA clearance for the whole group was unaltered by treatment. However, among those with relatively good pretreatment renal function (GFR greater than 70 ml/min per 1.73 m2), GFR increased at the end of 6 months' treatment (118.2 +/- 15 ml/min per 1.73 m2 versus 77.6 +/- 8.4 ml/min per 1.73 m2 in wash-out phase).(ABSTRACT TRUNCATED AT 250 WORDS)     

Nephrotic-range proteinuria associated with right atrial myxoma.

A case of right atrial myxoma presenting with right heart failure and proteinuria is described. Proteinuria was variable and this corresponded with the degree of systemic venous congestion. On one occasion the proteinuria was within the nephrotic range. There was no evidence of intrinsic renal pathology. The right heart failure and proteinuria resolved after tumour removal, suggesting that the etiology of urinary protein loss was a reversible increase in glomerular permeability.     

Lymphadenopathy of Kimura's disease

Kimura's disease is an important category of reactive lymphadenopathy in the Oriental population. The enlarged nodes are mostly located in the head and neck region. Salient pathological changes include florid germinal centers, Warthin-Finkeldey type polykaryocytes, vascularization of germinal centers, increased postcapillary venules in the paracortex, eosinophilic infiltration, and sclerosis. The pathology of Kimura's disease is quite different from that of angiolymphoid hyperplasia with eosinophilia (epithelioid hemangioma). Immunoperoxidase studies show IgE reticular networks in germinal centers. Nondegranulated surface IgE-positive mast cells are present in the paracortex. The authors propose that Kimura's disease represents an aberrant immune reaction to an as yet unknown stimulus. Although the individual histological features are nonspecific, the constellation of features is highly characteristic of Kimura's disease. Since lymphadenopathy can herald involvement of other tissues and the prognosis is excellent, accurate diagnosis of this disease in lymph node biopsies may spare the patients unnecessary radical surgery.     

Lymphadenopathy as the initial manifestation of histiocytosis X.

Seventeen cases of histiocytosis X presenting as lymphadenopathy, in which the initial diagnosis was based on lymph node biopsy, are reviewed, the characteristic histopathologic findings described, and the differential diagnosis discussed. Clinical evaluation reveals a broad spectrum of associated manifestations varying from solitary eosinophilic granuloma of lymph node to a disseminated Letterer-Siwe-like syndrome. Follow-up confirms the essentially benign nature of this disorder when defined by strict histologic criteria. The implications of these findings on the continuing controversy surrounding histiocytosis X are discussed.     

Renin-induced massive proteinuria in man.

A 30 year old man developed renovascular hypertension and extreme elevation of plasma renin activity. Daily proteinuria ranged from 13 to 31 g. There were no criteria for the diagnosis of malignant hypertension. A primary glomerulopathy was excluded by a basically normal renal biopsy from the unprotected kidney. On electron microscopy the epithelial cell foot processes were not fused, thus ruling out simultaneous lipoid nephrosis. The source of renin was removed by means of a left nephrectomy. Following the procedure the patient became normotensive, the renin values normalized and the proteinuria disappeared. The results suggest that renin can cause significant proteinuria in man.     

Giant bilateral perinephric tumour and overt proteinuria.

A 63-year-old man with type 2 diabetes mellitus and hypertensionpresented with increasing abdominal girth and foamy urine forthe previous 2 years. Impaired renal function (BUN 33 mg/dl,serum creatinine 2.3 mg/dl), hypoalbuminaemia (2.3 g/dl), overtproteinuria (11.2 g/day), microscopic haematuria (RBC 21-35/HPF)     

Hematuria and proteinuria in pediatric patient. Diagnostic approach

Some of the first clues suggestive of renal disease are hematuria and proteinuria, and when present in a child, deserve careful consideration. The clinical experience and diagnostic evaluations at a new renal unit are examined to familiarize the practicing urologists with the diagnostic approach which will generate the correct diagnosis. The indications and results of kidney biopsy in children are also presented.     

Adult height and proteinuria in type 2 diabetes.

BACKGROUND: Short stature has been shown to be associated with proteinuria in type 1 diabetes, but no data exist with respect to type 2 diabetes. The objective of the study was to investigate the relationship between final adult height and macroproteinuria in type 2 diabetic patients. METHODS: One hundred and forty-four consecutive type 2 diabetic patients (84 males, 60 females) with macroproteinuria were recruited into the study. For every patient, three diabetic controls matched for age, gender, and duration of diabetes were randomly selected. Height was measured in patients and controls to the nearest 0.5 cm. RESULTS: The mean height in men with macroproteinuria (n = 84) was 164.4 cm (SD 6.74) compared to 166.6 cm (SD 6.64) in controls (n = 252) (P < 0.01). The mean height in women with macroproteinuria (n = 60) was 150.6 cm (SD 5.20) compared to 152.5 cm (SD 5.78) in controls (n = 180) (P < 0.02). CONCLUSION: Short stature is associated with an increased risk of macroproteinuria in type 2 diabetic patients. We postulate that common genetic or environmental factors that affect final adult height might also predispose to the development of nephropathy.     

Simulated proteinuria and haematuria

In nephrology, like in other branches of medicine, falsification is motivated by a desire for profit or is an expression of some mental disorder. Three cases are described in which artificial proteinuria and haematuria were diagnosed by agarose gel electrophoresis of urinary proteins and a simulation and aggravation of renal disease was disclosed.