Futrakul P

Acute Glomerulonephritis Complicating Plasmodium Falciparum Infection

*** Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok, Thailand. ACUTE GLOMERUL(~i~IEPHRTTIS complicating Flc~.srno~liur~z falca~artcm infection has never been completely documented by immunologic or immunopathologic study, though Berger and associates in 1967 described three cases of acute glomerulonephritis in which renal biopsies were performed late, during the nephrotic state. The histopathologic studies showed a proliferative change with avascularity of the glomerular tu£ts.l 1

Enhanced Peritubular Capillary Flow and Renal Function Can Be Accomplished in Normoalbuminuric Type 2 Diabetic Nephropathy

Under common practice, treatment of diabetic nephropathy (DN) is usually initiated at late stage of CKD due to the insensitiveness of the available diagnostic markers. Such treatment fails to restore renal perfusion and function. This is due to the defective mechanism of vascular homeostasis and impaired nitric oxide production observed in late stage of DN. In contrast, the mechanism of vascular repair is adequately functional in early stage of DN (normoalbuminuria). In this study, we treated 50 normoalbuminuric diabetic patients with multidrug vasodilators, namely ACE inhibitor, angiotensin receptor blocker, ± calcium channel blocker in conjunction with correction of metabolic disorders for 24–36 months. Following the treatment, increment in peritubular capillary flow in response to vasodilators was observed, and thus supports the adequate role of vascular repair. In addition, increase in renal function documented in this study also implies that an effective preventive strategy to minimize end-stage renal disease can be accomplished in normoalbuminuric DN.

Significance of tubulointerstitial fibrosis in paediatric IgM nephropathy

Summary: The significance of tubulointerstitial fibrosis in paediatric patients with primary diffuse mesangial proliferative glomerulonephritis and IgM deposition (IgM nephropathy) has not been well documented. the clinical course, therapeutic response and final outcome of 35 patients in whom renal biopsies showed IgM nephropathy are reported. They have been subdivided into two groups according to the absence (19 patients: group I) or presence (16 patients: group II) of superimposed lesion of tubulointerstitial fibrosis. Clinical presentation was similar in both groups but the patients in group I were male predominant (2.8:1 vs 1: 1). 6/19 (31.6%) of the patients in group I and 1/16 (6.3%) in group II responded to corticosteroid, 11/19 (57.9%) in group I and 8/16 (50.0%) in group II had steroid dependent, whereas 2/19 (10.5%) in group I and 7/16 (43.7%) in group II had steroid resistant. About 42% of the patients in group I and 94% in group II required cyclophosphamide therapy by which similar response in both groups (approximately 75%) were observed. the steroid non‐responders and cyclophosphosphamide therapy among patients in group II were significantly higher (P<0.05) than the group I. At the latest assessment, 5/16 (31.3%) in group I and 7/14 (50%) in group II had impaired renal function. the follow‐up period in both groups were 3.1 ± 2.8 and 3.4 ± 2.9 years, respectively. In conclusion, the finding of tubulointerstitial fibrosis in a paediatric IgM nephropathy indicates an unfavourable therapeutic response.

Renal Dysfunctions in Glomerulonephropathy with Rapidly Declined Renal Failure

Eight patients aged between 5 and 26 years developed rapid deterioration of renal function and became oliguric/anuric with duration ranging from 1 to 21 days. The initial functional assessment revealed severe degree of glomerular, tubular, and vascular dysfunctions. The magnitude of renal dysfunction was quantified and expressed in terms of a clinical score. The degree of glomerular and tubular dysfunctions were inversely proportional to the renal plasma flow and peritubular capillary blood flow (PTCB), respectively. Similar findings have been observed in a variety of severe glomerulonephropathies. In this aspect, it is likely that the reduction of peritubular capillary blood flow and tubulointerstitial disease are interrelated. Further evidence to support the primary role of reduction of PTCB in inducing tubulointerstitial disease is provided by the following: (a) Reduction of PTCB is documented in mesangial proliferative nephrosis with steroid resistance prior to the detection of tubulointerstitial disease. (b) Ischemic insult can induce tubulointerstitial disease in experimental setting of renal artery occlusion in animal, (c) Improved tubular function can be achieved following the increase in PTCB with the enhanced renal perfusion therapy.

Renal hypoperfusion in nephrosis associated with focal segmental glomerulosclerosis

It has been speculated that idiopathic nephrosis associated with focal segmental glomerulosclerosis (NSFSGS) falls into two different expressions: a mild form with a normal or slightly impaired renal function and a slow progression and a severe form with progression to end-stage renal disease.-5 Patients of these two subsets have frequently shown a similar pattern of unresponsiveness to an 8 week course of prednisolone therapy. The diagnostic criteria are mainly dependent upon histopathological markers or serum variables such as serum creatinine or creatinine clearance representing the glomerular function. Such a diagnostic approach, in many instances, is unable to clearly differentiate between the two subsets of NS-FSGS. Inasmuch as structural change usually involves the three compartments of the nephron, namely the vascular, glomerular and tubulointerstitial compartments of the kidney, an assessment of function relating to other compartments besides the glomerulus would undoubtedly assist in quantifying the magnitude of clinical severity and in particular in differentiating between the mild and severe categories. To serve this purpose, an intrarenal haemodynamic study was performed in 15 patients with mild clinical manifestation and in 13 patients associated with severe renal dysfunction proning to enter end-stage renal disease. Using the previously described method6 the intrarenal haemodynamic of assessment the 15 mild cases of NS-FSGS revealed a mile reduction of renal plasma flow and glomerular filtration rate and a mild elevation of peripheral vascular resistance. In contrast, there were moderate to severe reductions of renal plasma flow and glomerular filtration rate and moderate to marked elevations of peripheral vascular resistance in the severe subset (Table 1). The functional defect documented by means of intrarenal haemodynamics was in agreement with the histopathological alteration in the vascular compartment between the two groups.

Renal dysfunction in glomerulonephropathy associated with rapid onset renal failure.

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.