Cases reported "Nephrosclerosis"

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1/50. The Ask-Upmark kidney: a form of ascending pyelonephritis?

    The case is presented of a young girl with recurrent urinary tract infection and vesico-ureteric reflux who developed a small scarred kidney and subsequently, hypertension. Pathologically, the renal changes were compatible with those of an Ask-Upmark kidney. The pathogenesis of the Ask-Upmark kidney is discussed. It is postulated that the lesion is not necessarily of congenital origin but may well be related to infection and intrarenal reflux, it is concluded that long-term follow-up of a young patient with a scarred kidney is indicated. ( info)

2/50. Severe hypertensive sequelae in a child with Seckel syndrome (bird-like dwarfism).

    We report a 19-year-old male with Seckel syndrome (bird-like dwarfism) who presents with malignant hypertension associated with hypertensive nephrosclerosis, dilated cardiomyopathy, and a ruptured cerebral artery aneurysm. Although end-organ injury due to chronic hypertension occurs frequently in adults, no previous reports of renal insufficiency due to hypertension exist in children or adolescents. We speculate that this patient may have been particularly prone to hypertensive end-organ injury due to his extreme short stature. ( info)

3/50. Disposition of [G-(3)H]paclitaxel and cremophor EL in a patient with severely impaired renal function.

    In the present work, we studied the pharmacokinetics and metabolic disposition of [G-(3)H]paclitaxel in a female patient with recurrent ovarian cancer and severe renal impairment (creatinine clearance: approximately 20 ml/min) due to chronic hypertension and prior cisplatin treatment. During six 3-weekly courses of paclitaxel at a dose level of 157.5 mg/m(2) (viz. a 10% dose reduction), the renal function remained stable. Pharmacokinetic evaluation revealed a reproducible and surprisingly high paclitaxel area under the plasma concentration-time curve of 26.0 /- 1.11 microM.h (mean /- S.D.; n = 6; c.v. = 4.29%), and a terminal disposition half-life of approximately 29 h. Both parameters are substantially increased ( approximately 1.5-fold) when compared with kinetic data obtained from patients with normal renal function. The cumulative urinary excretion of the parent drug was consistently low and averaged 1.58 /- 0.417% ( /- S.D.) of the dose. Total fecal excretion (measured in one course) was 52.9% of the delivered radioactivity, and mainly comprised known mono- and dihydroxylated metabolites, with unchanged paclitaxel accounting for only 6.18%. The plasma area under the plasma concentration-time curve of the paclitaxel vehicle Cremophor EL, which can profoundly alter the kinetics of paclitaxel, was 114.9 /- 5.39 microl.h/ml, and not different from historic data in patients with normal or mild renal dysfunction. Urinary excretion of Cremophor EL was less than 0.1% of the total amount administered. These data indicate that the substantial increase in systemic exposure of the patient to paclitaxel relates to decreased renal metabolism and/or urinary elimination of polar radioactive species, most likely lacking an intact taxane ring fragment. ( info)

4/50. Myeloperoxidase-antineutrophil cytoplasmic antibody-associated glomerulonephritis superimposed on biopsy-proven diabetic nephrosclerosis.

    We present a case of myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA)-associated glomerulonephritis with diabetic nephrosclerosis, diagnosed by serial renal biopsies within a short period. A 78-year-old man with renal insufficiency, who had been diagnosed with diabetic nephrosclerosis by renal biopsy 9 months earlier, was admitted to the hospital for dyspnea and rapid deterioration of renal function. The titer of serum MPO-ANCA was high, and the second renal biopsy confirmed the presence of necrotizing glomerulonephritis with crescents. methylprednisolone pulse therapy followed by oral administration of prednisolone led to resolution of respiratory symptoms and reversal of MPO-ANCA. Renal function did not improve, however, necessitating hemodialysis. A review of the literature showed several cases of necrotizing glomerulonephritis superimposed on diabetic nephropathy but only a few reported cases of MPO-ANCA glomerulonephritis associated with diabetic nephrosclerosis. Diabetic patients who show rapid deterioration of renal function should undergo renal biopsy to determine the concomitant presence, if any, of other glomerular diseases and to prevent life-threatening systemic involvement. ( info)

5/50. The pathophysiology and management of renal bone disease in dialysis patients.

    As renal function declines, changes in mineral metabolism occur including phosphate retention, calcitriol deficiency, and the development of secondary hyperparathyroidism. Renal bone disease related to disordered mineral metabolism may result in increased patient morbidity and mortality. Uncontrolled parathyroid hormone (PTH) secretion will result in osteitis fibrosa, a high turnover bone disease. The use of calcium and aluminum-based phosphate binders and vitamin d sterols may contribute to the development of low turnover bone diseases such as osteomalacia and aplastic bone disease. Prevention and control of renal bone disease is an important goal for the interdisciplinary health care team. This paper discusses disordered mineral metabolism and its relationship to renal bone disease. Case studies illustrate the development and treatment of renal bone disease related to secondary hyperparathyroidism and aluminum intoxication. ( info)

6/50. A patient with apolipoprotein e2 variant (Q187E) without lipoprotein glomerulopathy.

    Four apolipoprotein (apo) E variants have been reported to be associated with lipoprotein glomerulopathy (LPG), which is characterized by type III hyperlipoproteinemia (type III HLP) and proteinuria and frequently leads to nephrotic syndrome. We report the histologic findings in the kidneys of a type III HLP patient with an apo E variant, apo E Toranomon, in which the glutamine at residue 187 in apo E is substituted by glutamic acid (Q187E). The patient also had type 2 diabetes mellitus. No evidence of lipoprotein thrombi suggestive of LPG was detected, however, and the histologic diagnosis was diabetic nephrosclerosis. This unique case illustrates that not all apo E variants result in LPG, and the location of mutations in the apo E protein is one of the important determinants for the development of LPG. ( info)

7/50. Characteristics of the tumours of the urinary tract in patients with endemic nephropathy.

    The authors have studies in detail the development of tumours in the urinary tract of patients with endemic nephropathy (EN). They have found tumours in about 40% of these patients. They have performed operations for tumours of the urinary tract in 88 patients with EN, with a different localization in the upper part of the urinary tract. In 10% of the cases they have found bilateral tumours. The histological examination has revealed papillary tumours of a malignant character. They have shown specific symptoms of these tumours, not found with other tumours of the urinary tract. The main symptom is renal insufficiency which causes the death of the patients. The evolution of these tumours is comparatively slow and the nature of EN has determined the operative approach of the authors, a radical operation with haemodialysis when indicated. The paper is illustrated with four typical cases. ( info)

8/50. Calcification in an angiomyolipoma: a case report.

    A patient with tuberous sclerosis and angiomyolipoma of both kidneys is described in whom both tumors demonstrated associated calcification. This finding has not been previously stressed in the literature and is important in that ignorance of its occurence in this tumor might result in an error of diagnosis and nephrectomy in a patient who can ill-afford the loss of renal parenchyma. ( info)

9/50. Pseudohyperphosphatemia in a hyperphosphatemic hemodialysis patient.

    hyperphosphatemia is a predictable consequence of end-stage renal disease. Pseudohyperphosphatemia is a spurious elevation of serum phosphate in samples containing a substance that interferes with the laboratory assay for phosphate. The most common cause is a paraprotein in disorders such as Waldenstrom's macroglobulinemia and multiple myeloma. We report here a case of pseudohyperphosphatemia in a hyperphosphatemic patient with end-stage renal disease on long-term hemodialysis caused by a saline solution containing phosphorus used to dilute the patient's serum sample in the clinical chemistry laboratory. Investigations showed that the phosphorus most likely was introduced at the time of saline manufacture. Pseudohyperphosphatemia resulting from the manufacture and distribution of saline-containing phosphorus could be a cause of abnormally high serum phosphate measurements in hyperphosphatemic dialysis patients whose serum samples must be diluted in the laboratory. Such spuriously elevated results can lead to inappropriate changes in medications and subject patients to additional hemodialysis treatments. ( info)

10/50. nephrosclerosis postpartum and in women taking oral contraceptives.

    The condition of a patient with postpartum nephrosclerosis improved during heparin therapy. review of the literature disclosed 29 other patients with the same histopathologic characteristics, eight of whom also recovered substantial renal function after anticoagulation therapy. Also reported is a patient in whom renal failure occurred while she was taking oral anovulatory agents. Renal biopsy specimen showed the same histopathologic features, which raises the question of similar factors mediating the expression of this disease. We suggest a uniform terminology for this syndrome, either postpartum nephrosclerosis or nephrosclerosis in women taking oral contraceptives. ( info)
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