title: Renal dysfunction in glomerulonephropathy associated with rapid onset renal failure.
abstract: Eight patients between the ages of 5 and 26 years developed a rapid decline of renal function with a period of oliguria or anuria which ranged between 1 and 21 days. The initial assessment of renal function revealed a severe degree of glomerular, tubular, and vascular abnormalities. The magnitude of the renal dysfunction was quantified and expressed in terms of a clinical score. The degree of glomerular and tubular dysfunction was inversely proportional to the renal plasma flow and peritubular capillary blood flow, respectively. Similar findings have been observed in a variety of other glomerulonephropathies where a relationship exists between the reduction of peritubular capillary blood flow and the severity of the tubulointerstitial disease. Evidence to support the position that the reduction of peritubular capillary blood flow plays a primary role in inducing tubulointerstitial disease is as follows: (i) A reduction of peritubular capillary blood flow has been documented in mesangial proliferative nephrosis with steroid resistance prior to the detection of tubulointerstitial disease. (ii) Ischemic insults are capable of inducing tubulointerstitial disease in the experimental setting of renal artery occlusion in animals. (iii) As demonstrated in the present report, an improvement of tubular function can be achieved following an increase in peritubular capillary blood flow with therapy designed to enhance renal perfusion.
authors.affiliation: Faculty of Medicine of Chulalongkorn University, Chulalongkorn Medical School Hospital, Bangkok, Thailand.
authors.forename: N
authors.initials: N
authors.lastname: Futrakul
authors.forename: C
authors.initials: C
authors.lastname: Pochanugool
authors.forename: V
authors.initials: V
authors.lastname: Sitprija
authors.forename: V
authors.initials: V
authors.lastname: Singkhwa
authors.forename: P
authors.initials: P
authors.lastname: Futrakul
authors.forename: S
authors.initials: S
authors.lastname: Yenrudi
authors.forename: R
authors.initials: R
authors.lastname: Sensirivatana
authors.forename: D
authors.initials: D
authors.lastname: Watana
authors.forename: M
authors.initials: M
authors.lastname: Poshyachinda
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy; D000293:Adolescent; D000328:Adult; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000925:Anticoagulants / Q000627:therapeutic use; D001002:Anuria / Q000150:complications / Q000503:physiopathology; D001783:Blood Flow Velocity; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002648:Child; D002675:Child, Preschool; D017315:Cilazapril / Q000627:therapeutic use; D004176:Dipyridamole / Q000627:therapeutic use; D004359:Drug Therapy, Combination; D005919:Glomerular Filtration Rate; D005921:Glomerulonephritis / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D017275:Isradipine / Q000627:therapeutic use; D007668:Kidney / Q000187:drug effects / Q000473:pathology* / Q000503:physiopathology; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D017595:Renal Plasma Flow; D016896:Treatment Outcome; D014655:Vascular Resistance
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000925:Anticoagulants; D002121:Calcium Channel Blockers; D010975:Platelet Aggregation Inhibitors; D017315:Cilazapril; D004176:Dipyridamole; D006493:Heparin; D017275:Isradipine