Chronic renal failure in Thai children: etiology, cost, and outcome.

We studied the epidemiology, cost and outcome of chronic renal failure (CRF) in Thai children by sending questionnaires to all university hospitals, all government general service hospitals and all pediatric nephrologists in the country. A total of 238 cases (107 from 8 university hospitals and 131 from 70 government general service hospitals) were diagnosed from 1996 to 1998. Mean age of the patients was 8.3 +/- 4.9 yr, male to female ratio was 1.4:1. Congenital KUB anomalies (obstructive uropathy and hypo/dysplasia) were the main causes of CRF in these patients, especially in the under five age group. Only a small number of patients received renal replacement therapy (chronic dialysis and kidney transplant) and the mortality rate was 18.7 per cent in university hospitals. Renal transplantation was performed in only 5 patients in 2 pediatric units and another 2 patients in adult renal units. The outcome of renal transplantation in this small group of patients was very satisfactory. The cost of CRF treatment in children was comparable to adults. The main problems in the management of CRF in Thai children included the lack of experienced personnel, lack of equipment and funding. We conclude that in order to improve the care of CRF in Thai children, a training program for health personnel and budget allocation should be established.

Renal perfusion and disease progression.

The pathogenetic concept of renal hyperperfusion and hyperfiltration in inducing glomerular pathology and disease progression documented in the renal ablation model in experimental animals to mimic renal disease with reduced nephron mass has recently been challenged. In contrast to the above, the intrarenal hemodynamic study in a variety of chronic glomerulonephropathies reveals a unique characteristic of renal hypoperfusion rather than hyperperfusion. This is associated with an elevated renal arteriolar resistance and reductions in renal plasma flow and peritubular capillary blood flow. The magnitude of reduction in peritubular capillary blood flow is inversely proportional to the degree of tubulointerstitial disease and tubular dysfunction. A progressive reduction in the vascular space due to nonvascular expansion with disease progression supports the concept of hypoperfusion of a whole kidney as well as a single nephron. In accordance with the renal ablation model and early diabetes mellitus, a similar hypoperfusion pattern is also subsequently observed in the chronic stage of renal ablation model in animals and late diabetic nephropathy. The disparity between the hyperperfusion and hypoperfusion in inducing renal disease progression can be enlightened by the Noble Truth of Lord Buddha stating "The Middle Tract is The Balance of Nature". Further support of this conceptual view of renal hypoperfusion as a determinant of tubulointerstitial disease and disease progression is in accordance with the therapeutic benefit with an enhanced-renal-perfusion formula per se in a variety of chronic glomerulonephropathies.

Intrarenal hemodynamic abnormality in severe form of glomerulonephritis: therapeutic benefit with vasodilators.

Intrarenal hemodynamic and tubular function has been assessed in 16 patients who presented clinically with hypertension, hematuria and severe renal functional impairment. Twelve of these 16 patients had histopathologic classification as DPGN (3 cases), MPGN (3 cases) and FSGS (6 cases). The initial assessment of intrarenal hemodynamics in 11 patients revealed strikingly increased afferent (RA) and efferent arterioles (RE), filtration fraction (FF), intraglomerular capillary hydrostatic pressure (PG), whereas, there was marked reduction in renal plasma flow (RPF), in ultrafiltration coefficient (KFG) and in glomerular filtration rate (GFR). Tubular transporting defect as being reflected by enhanced fractional excretions of solutes was also observed. Both enhanced TXB2 production and diminished PGI2 may be in part responsible for the marked reduction of RPF and elevated intrarenal resistance. In light of the preceding intrarenal hemodynamics alteration, therapeutic intervention with vasodilators consisting of dipyridamole, calcium channel blocker and angiotensin convertase inhibitor has been accomplished with clinical improvement in glomerular and tubular functions following the improvement in intrarenal hemodynamics. Thus, this abnormal intrarenal hemodynamics renders a supportive view of the hemodynamically mediated glomerulo-tubulo-interstitial injury to be central to the pathogenetic mechanism.