FP350DIFFUSE MICROVASCULAR NEPHROPATHY AS A CAUSE OF CHRONIC RENAL FAILURE

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INTRODUCTION: While random and patchy atherosclerotic changes of intermediate size intrarenal arteries can lead to renal failure by microinfarctions, diffuse degenerative involvement of small pre-glomerular vessels is not presently recognized as a cause of circulatory damage ending in progressive decrease of GFR. This entity could belong to the unknown causes of CRF presently amounting to some 20% of the patients. The direct, pathogenetic role exerted by a diffuse damage of renal microcirculation could be expected to impair glomerular perfusion because of the increased resistance to blood flow in pre-glomerular vessels. To the extent that these changes can be evidenced by renal Ecodoppler measurements of intra-parenchymal resistance indexes (RI), this putative entity can be detected in patients with normal or non-stenotic renal arteries. Thus, this entity could be the renal counterpart of “Microvascular Angina ", a form of ischemic heart disease in which the coronary arteries (equivalent to the renal arteries in our hypothesis) do not show hemodynamically significant stenoses, while the ischemic damage is born solely by the myocardial microcirculation. We specifically addressed this issue in the present study. METHODS: We retrospectively evaluated 1563 patients with GFR between 89 and 15 mL/min who had been followed by the Nephrology Clinics of the Integrated University Hospital of Udine (Italy) between January 1st 1991 and November 28th 2017. From this group, we selected patients in whom the renal Ecodoppler measurements had shown bilaterally RI ≥ 0.7 in the absence of each of the followings: a) glomerular disease (proteinuria <di 130 mg/day, albuminuria <20 mg/day); b) systemic diseases with renal involvement; c) active or previous tubular disease (beta2 microglobulin <193 micrograms/L, serum uric acid and excreted fraction of sodium no greater than expected for the degree of renal failure); d) Polycystic kidney disease; e) stenosis of one or both renal arteries. Multiple correlations were performed between data obtained by renal Ecodoppler measurements and renal functional indices. RESULTS: The group was composed by 131 patients (8.4% of the total, 73 males and 58 females, mean age 76 years), who fully satisfied the inclusion criteria. A statistically significant correlation was found only between GFR and IR (R=0.31, p <0.001). No statistically significant correlations were found, among others, between GFR and 24-hour proteinuria (R=0.11, p=0.22) and between GFR and 24-hour beta2microglobinuria (R=0.11, p=0.22). CONCLUSIONS: Diffuse Chronic Microvascular Nephropathy could progress to CRF through mechanisms different from glomerular hyper-perfusion. Being caused by increased pre-glomerular vascular resistance, it is expected to lead to glomerular under-perfusion, which could trigger increased efferent vascular resistance to maintain intra-glomerular pressure. Thus, while hyper-perfusion could act through increased parietal glomerular capillary stress, the hypo-perfusion pathway could progress through increased glomerular capillary pressure with dampened pulse wave profile, such that vasodilating the efferent arterioles could further impair GFR. This suggests curbing the use of ACE-inhibitors and angiotensin II receptor blockers in this subset of patients. The definition of this clinical entity requires more detailed experimental and clinical observations.

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