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At least 1,297 records · Page 72Linked to original sources
PubMed1979

Thrombocytopenia in obstetric syndromes. A review.

Thrombocytopenia is a phenomenon sometimes observed in connection with various obstetric syndromes. Many times it appears clinically to be a comparatively benign complication of an otherwise significant disease. In some cases, however, it may be a clue to serious disease and its pathophysiology. The subject of thrombocytopenia induced by or related to various obstetric syndromes is reviewed and comments offered regarding the significance of the observation of platelet deficiency in these conditions.

Adolescent↗
PubMed1976

Erythrocytosis associated with diffuse parenchymal lesions of the kidney.

Thirteen patients with diffuse parenchymal disease of the kidney and erythrocytosis are reported. In five the haematocrit was only minimally elevated because of an associated increase in plasma volume. The erythrocytosis in three patients was of particular interest: (1) transient appearance in a 23-year-old man with glomerulonephritis; (2) persistence despite the partial remission of nephrotic state in a 19-year-old man; (3) appearance following removal of a nephrosclerotic kidney from a 54-year-old woman. Because an associated expansion of plasma volume is not uncommon with parenchymal renal disease, it is suggested that the only reliable screening method for renal erythrocytosis is direct measurement of red cell volume.

Adult↗
PubMed1976

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.

Child↗
PubMed1984

Pulse methylprednisolone therapy in severe idiopathic childhood nephrotic syndrome.

The effect of methyl prednisolone therapy (PM) was studied in 18 children with severe idiopathic nephrotic syndrome (NS). Eight patients were defined as "corticosteroid-resistant" because there was no response to treatment after a minimum of 4 weeks of 2 mg/kg/day of prednisone; 10 patients had a corticosteroid-dependent NS with frequent relapses which occurred under a high threshold dose of prednisone (1 mg/kg/day). Each patient received 4-6 pulses of 1 g/1.73 m2 methylprednisolone. Tolerance was generally good. PM therapy permitted a more rapid remission than oral prednisone (average 9 +/- 4 days vs. 22 +/- 9 days). Remission occurred in 5 of the 8 corticosteroid-resistant patients three of these 5 patients developed corticosteroid-dependent NS. For the children with a corticosteroid-dependent nephrotic syndrome, PM therapy did not affect the threshold dose of prednisone.

Adolescent↗
PubMed2005

Tranilast prevents the progression of experimental diabetic nephropathy through suppression of enhanced extracellular matrix gene expression.

The present study was performed to investigate the effects of the antiallergic drug tranilast on the development of diabetic nephropathy in streptozotocin (50 mg/kg)-induced diabetic spontaneously hypertensive rats (SHR). Diabetic SHR were given standard chow or chow containing tranilast at a dose of 1400 mg/kg for 24 weeks. The effects of tranilast on urinary albumin excretion, mesangial expansion, expression of transforming growth factor-beta (TGF-beta) and type I collagen mRNAs, number of anionic sites on the glomerular basement membrane (GBM), and urinary TGF-beta and 8-hydroxy-2'-deoxyguanosine (8-OHdG) excretion were assessed. Tranilast did not affect the blood glucose concentration or blood pressure in diabetic SHR. Urinary albumin excretion rate and creatinine clearance were markedly increased in diabetic SHR. Tranilast treatment decreased albuminuria and hyperfiltration. Tranilast inhibited the diabetes-induced expansion of mesangial and tuft areas, as well as the increase in urinary TGF-beta and 8-OHdG excretion, loss of anionic sites of GBM, and overexpression of TGF-beta as determined immunohistochemically. The levels of TGF-beta and type I collagen mRNA expression were increased in the renal cortex in untreated diabetic SHR at 24 weeks, as determined by real-time quantitative polymerase chain reaction. Tranilast treatment inhibited the up-regulation of TGF-beta and type I collagen mRNA expression by 65 and 36%, respectively, in diabetic SHR. In conclusion, tranilast decreased albuminuria by suppressing glomerular hyperfiltration, mesangial expansion, and loss of the charge barrier via regulation of extracellular matrix gene expression and oxidative stress. Tranilast may be clinically useful in the treatment of diabetic nephropathy.

Albuminuria↗