Abstract

BackgroundWe investigated the renoprotective ability of healthy people against kidney stone formation. To clarify intratubular crystal kinetics and processing in human kidneys, we performed a quantitative and morphological observation of nephrectomized renal parenchyma tissues.MethodsClinical data and pathological samples from 60 patients who underwent radical nephrectomy for renal cancer were collected from June 2004 to June 2010. The patients were retrospectively classified as stone formers (SFs; n = 30, kidney stones detected by preoperative computed tomography) and non-stone formers (NSFs; n = 30, no kidney stone history). The morphology of parenchymal intratubular crystals and kidney stone-related gene and protein expression levels were examined in noncancerous renal sections from both groups.ResultsSFs had a higher smoking rate (P = 0.0097); lower red blood cell, hemoglobin, and hematocrit values; and higher urinary red blood cell, white blood cell, and bacterial counts than NSFs. Scanning electron microscopy revealed calcium-containing crystal deposits and crystal attachment to the renal tubular lumen in both groups. Both groups demonstrated crystal transmigration from the tubular lumen to the interstitium. The crystal diffusion analysis indicated a significantly higher crystal existing ratio in the medulla and papilla of SFs and a significantly higher number of papillary crystal deposits in SFs than NSFs. The expression analysis indicated relatively high osteopontin and CD68, low superoxide dismutase, and significantly lower Tamm–Horsfall protein expression levels in SFs. Multivariate logistic regression analysis involving the above factors found the presence of renal papillary crystals as a significant independent factor related to SFs (odds ratio 5.55, 95% confidence interval 1.08–37.18, P = 0.0395).ConclusionsRegardless of stone formation, intratubular crystals in the renal parenchyma seem to transmigrate to the interstitium. SFs may have reduced ability to eliminate renal parenchymal crystals, particularly those in the papilla region, than NSFs with associated gene expression profiles.

Highlights

  • We investigated the renoprotective ability of healthy people against kidney stone formation

  • Since the introduction of extracorporeal shock-wave lithotripsy in 1980, [1] fewer opportunities for open surgery have led to fewer chances for pathological investigations of kidney stone formation (KSF) using human kidney parenchymal tissue

  • The factors currently considered to affect calcium kidney stone formation are stone matrix proteins, cell injury caused by oxidative stress, monocyte/macrophage induction, and urinary stone inhibitors

Read more

Summary

Introduction

We investigated the renoprotective ability of healthy people against kidney stone formation. To clarify intratubular crystal kinetics and processing in human kidneys, we performed a quantitative and morphological observation of nephrectomized renal parenchyma tissues. The factors currently considered to affect calcium kidney stone formation are stone matrix proteins, cell injury caused by oxidative stress, monocyte/macrophage induction, and urinary stone inhibitors. We reported renal intratubular crystal elimination in a mouse model, increased expression of macrophage-related inflammatory genes in a DNA microarray analysis of stone-forming kidneys, [13] and phagocytosis of interstitial crystals by macrophages under transmission electron microscopy, [19] suggesting the kidney stone-preventive ability of macrophages by crystal processing. Tamm–Horsfall protein (THP), a urinary inhibitor of stone formation, has been studied because THP-deficient mice demonstrate spontaneous calcium crystal formation [21]

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call