Browsing by Author "Kyaw Wynn"

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    Hypertension among patients with glomerulonephritis in NOGH
    (1994-01-01) Mya Mya Win; Aung Saw Naung; Mie Mie; Kyaw Wynn
    Hypertension is an important cardiovascular disease and a recognized accompaniment of glomerulonephritis. The aim of this study is to determine the incidence of hypertension among patients with glomerulonephritis and determine the various histological types which are associated with hypertension in North Okkalapa General Hospital. The period of study is from 1 December 1992 to 25 October 1993. All patients with biopsy proven glomerulonephritis were included in the study. There were 80 patients with glomerulonephritis and (53 percent) were found to be hypertensive. (65 percent) of those patients with glomerulonephritis who were hypertensive had mesangiocapillary proliferative glomerulonephritis followed by mesangial proliferative glomerulonephritis (43 percent). Oedema, the hallmark of nephritis, was absent in (11 percent) of the hypertensive patients. There were four patients with hypertension associated with pregnancy. (75 percent) had mesangiocapillary proliferative glomerulonephritis. Mesangiocapillary glomerulonephritis is the histological type most commonly associated with glomerulonephritis. As hypertension was the sole presenting feature in (4 percent) of patients with glomerulonephritis, glomerulonephritis should be considered in all young patients with hypertension.
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    Renal involvement in viper bite
    (1994-01-01) Paing Soe; Kyaw Wynn; Aye Thein
    Acute renal failure in viper bite is sometimes due to prerenal causes and sometimes by renal causes per se. Some facts, however, remain in doubt with regard to renal histological findings and the precise pathogenesis of established ARF. 28 viper bite cases admitted to renal and dialysis unit, Department of Nephrology, Yangon General Hospital, over a period of two years were biopsied and their clinical and biochemical parameters evaluated. This study reveals that ARF in viper bite is attributable to a total nephron failure-a combination of glomerular, tubulointerstitial and vascular nephropathies rather than due simply to acute tubular necrosis. A combination of several different mechanisms may operate in the pathogenesis. The possible pathogenetic mechanisms are being discussed. How different mechanisms operate at different times may call for further sophisticated studies.