Peritubular Capillary Flow and Tubular Function in Idiopathic Nephrotic Syndrome

Futrakul, Narisa; Yenrudi, Saowanee; Futrakul, Prasit; Cherdkiadtikul, Thumronkprawat; Laohapaibul, Aimon; Futrakul, Sithivudh; Sensirivatana, Rachanee

doi:10.1159/000045654

Cited by 8 publications

(4 citation statements)

References 5 publications

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“…Improvement in CCr and FE Mg is delineated in this study along with the enhancement of RPF and PTCF. Inasmuch as FE Mg correlates with the tubulointerstitial fibrosis [13] and inversely correlates with the PTCF, [14] the improvement in FE Mg following the treatment implies that there is likely a regression of tubulointerstitial injury. This view is further supported by the observation that suppression of angiotensin II formation in the kidney can be achieved by the combination of angiotensin II receptor antagonist and angiotensin converting enzyme inhibitor.…”

Section: Discussionmentioning

confidence: 99%

Treatments of Hemodynamic Maladjustment and Oxidative Stress Prevent Renal Disease Progression in Chronically Severe Glomerulonephritides

et al. 2003

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Hemodynamic maladjustment is a unique observation in chronically severe glomerulonephritides. It is characterized by a markedly elevated efferent arteriolar resistance (RE), an elevated intraglomerular hydrostatic pressure (PG) and a markedly decreased renal plasma flow (RPF), and peritubular capillary flow (PTCF). A correction of such hemodynamic maladjustment can be accomplished by administering a combination of vasodilators (angiotensin receptor antagonist, angiotensin converting enzyme inhibitor, and calcium channel blocker) in 14 chronic glomerulonephritides with severe renal function impairment (mean serum creatinine 3.6 + 1.3 mg/dL). Doses titration aim for maximal renal perfusion effect (increased RPF, PTCF) or maximal renal function improvement (increased CCr, reduced FE Mg) usually higher than needed for maximal blood pressure reduction. Evidence of oxidative stress is also corrected with high doses of vitamins C and E. After a mean period of treatment for 13.5 months, improvements in CCr (pre R(x) 22 +/- 10 vs. post R(x) 32 +/- 13 mL/min/1.73 m2), and FE Mg (pre R(x) 11.9 +/- 4% vs. post R(x) 10 +/- 3%) were observed in conjunction with the improvement in intrarenal hemodynamics namely RPF (pre R(x) 201 +/- 71 vs. post R(x) 288 +/- 99 mL/min/1.73 m2), PTCF (pre R(x) 161 +/- 57 vs. post R(x) 242 +/- 90 mL/ min/1.73 m2), PG (pre R(x) 56.7 +/- 0.5 vs. post R(x) 51 +/- 0.1 mm Hg), and RE (pre R(x) 12085 +/- 6503 vs. post R(x) 6550 +/- 1872 dyne.s.cm(-5)).

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Section: Discussionmentioning

confidence: 99%

Treatments of Hemodynamic Maladjustment and Oxidative Stress Prevent Renal Disease Progression in Chronically Severe Glomerulonephritides

et al. 2003

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“…The titration of the doses of vasodilators is mainly dependent upon the values of CCr, FE Mg and total urinary protein. FE Mg appears to be a very sensitive and practicable marker for clinical severity [5] as well as for the hemodynamic status, [30] since it correlates directly with the magnitude of tubulointerstitial fibrosis and inversely with the PTCF.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic Maladjustment and Disease Progression in Nephrosis with FSGS

Futrakul

Siriviriyakul²,

Deekajorndej³

et al. 2004

Renal Failure

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Idiopathic nephrotic syndrome (NS) associated with focal segmental glomerulosclerosis (FSGS) and severe renal function impairment is usually refractory to the conventional treatment and progresses to end-stage renal disease. Herein, we reported 10 patients with NS-FSGS who had initially had CCr 34 +/- 12 mL/min/1.73 m2 (normal 120 mL/min/1.73 m2), FE Mg 7.8 +/- 2.6% (normal 2.2%), 24-h urinary protein 3.1 g (normal <200 mg) and been followed up for over 10 years. The initial intrarenal hemodynamic study revealed a marked elevation of efferent arteriolar resistance (RE 17289 +/- 8636 dyne x s x cm(-5); normal 3000 dyne x s x cm(-5)), intraglomerular hypertension (PG 57 +/- 1 mm Hg; normal 52 mm Hg), hyperfiltration (FF 0.24; normal 0.2), marked reductions in GFR 35 +/- 17 mL/min/1.73 m2, renal plasma flow (RPF 159 +/- 61 mL/min/1.73 m2; normal 600 mL/min/1.73 m2) and peritubular capillary flow (PTCF 123 +/- 57 mL/min/1.73 m2; normal 480 mL/min/1.73 m2). Such a hemodynamic alteration indicated a hemodynamic maladjustment with a preferential constriction at RE. Treatment consists of multidrugs, namely angiotensin converting enzyme inhibitor, calcium channel blocker, antiplatelet and anticoagulant, with or without angiotensin II receptor antagonist. Following the treatment, correction of hemodynamic maladjustment has been achieved which is characterized by reductions in RE 6046 +/- 2191 dyne x s x cm(-5), PG 52 +/- mm Hg, FF 0.19 +/- 0.1 and increments in RPF 341 +/- 118 mL/min/1.73 m2, PTCF 280 +/- 106 mL/min/1.73 m2 and GFR 64 +/- 17 mL/min/1.73 m2. Coinciding with hemodynamic improvement, there has been a steadily increased creatinine clearance and improvement in FE Mg 4.3 +/- 2.6% and suppression of proteinuria 0.29 +/- 0.4 g/24 h after the period of follow-up of greater than 10 years.

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“…In this essence, a mild elevation of FE Mg indicates the presence of a small magnitude of tubulointerstitial fibrosis, whereas the higher elevation of FE Mg reflects the greater magnitude of tubulointerstitial firosis. In addition, FE Mg has also been demonstrated to inversely correlate with the peritubular capillary flow reduction in type 2 diabetic nephropathy [8] and idiopathic nephrotic syndrome [9,10].…”

Section: Indices Indicating Early Renal Mi-crovascular Disease In Diamentioning

confidence: 99%

Indices Indicating Early Renal Microvascular Disease in Diabetes

Futrakul¹,

Futrakul²

2011

TOBIOMJ

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Abstract:Renal microvascular disease is crucial to renal disease progression. Renal microvascular disease in late stage diabetic nephropathy is associated with defective angiogenesis and fails to respond to vasodilator treatment. Recognition of early renal microvascular disease is necessary, since in this stage, the vascular homeostasis is adequately functional and responsive to vasodilator treatment. Indices that can screen early renal microvascular disease include creatinine clearance or glomerular filtration rate, renal plasma flow or peritubular capillary flow and fractional excretion of magnesium (FE Mg).

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Peritubular Capillary Flow and Tubular Function in Idiopathic Nephrotic Syndrome

Cited by 8 publications

References 5 publications

Treatments of Hemodynamic Maladjustment and Oxidative Stress Prevent Renal Disease Progression in Chronically Severe Glomerulonephritides

Treatments of Hemodynamic Maladjustment and Oxidative Stress Prevent Renal Disease Progression in Chronically Severe Glomerulonephritides

Hemodynamic Maladjustment and Disease Progression in Nephrosis with FSGS

Indices Indicating Early Renal Microvascular Disease in Diabetes

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