Evaluation of Renal Oxygenation and Hemodynamics in Patients with Chronic Kidney Disease by Blood Oxygenation Level-dependent Magnetic Resonance Imaging and Intrarenal Doppler Ultrasonography

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Abstract

Introduction: The basic pathophysiologic derangement of chronic kidney disease (CKD) begins with the loss of nephrons, leading to renal hemodynamic changes, eventually causing a reduced nephron count and renal hypoxia. The purpose of this study was to observe the renal oxygenation and renal hemodynamics of patients with CKD using blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) and intrarenal Doppler ultrasonography (IDU). Methods: The study enrolled 39 patients with stage 1–4 CKD and 19 healthy volunteers (HVs). Based on their estimated glomerular filtration rate (eGFR), CKD patients were divided into 2 subgroups: a mild renal impairment (MI) group and a moderate to severe renal impairment (MSI) group. We monitored the participants’ mean cortical T2* (COT2*) and mean medullary T2* (MET2*) values on BOLD-MRI, and measured the peak systolic velocities (PSVs), end-diastolic velocities (EDVs), renal resistive index (RI), and kidney length by IDU. We also recorded clinical indicators such as age, sex, body mass index (BMI), 24-h urinary protein (24-h Upr), serum creatinine (sCr), blood urea nitrogen (BUN), and eGFR. BOLD-MRI, IDU measurements, and the clinical indicators were compared in CKD patients and HVs by the analysis of variance and Kruskal-Wallis H test. Spearman’s correlation was used to assess the relationship between data from BOLD-MRI and IDU and clinical indicators. Results: The COT2* values were significantly higher than the MET2* values in the HV, MI, and MSI groups. COT2*, MET2*, EDV, PSV, and kidney length gradually decreased in the HV, MI, and MSI groups (all p < 0.05), whereas RI and 24-h Upr gradually increased (both p < 0.05). Spearman correlation analysis showed that COT2* and MET2* were significantly positively correlated with eGFR, PSV, EDV, and kidney length but were significantly negatively correlated with sCr, BUN, and 24-h Upr (all p < 0.05). There was no correlation observed between the COT2* and MET2* and the RI and BMI values. Conclusions: Renal oxygenation and blood flow velocities were found declined as the CKD stage progressed. The BOLD-MRI and IDU techniques may have clinical value by measuring intrarenal oxygenation and renal blood perfusion to judge the severity of renal damage in patients with CKD.

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Chronic Kidney Disease.

Angela Webster, Evi V Nagler, Rachael Morton … (2017)

The definition and classification of chronic kidney disease (CKD) have evolved over time, but current international guidelines define this condition as decreased kidney function shown by glomerular filtration rate (GFR) of less than 60 mL/min per 1·73 m(2), or markers of kidney damage, or both, of at least 3 months duration, regardless of the underlying cause. Diabetes and hypertension are the main causes of CKD in all high-income and middle-income countries, and also in many low-income countries. Incidence, prevalence, and progression of CKD also vary within countries by ethnicity and social determinants of health, possibly through epigenetic influence. Many people are asymptomatic or have non-specific symptoms such as lethargy, itch, or loss of appetite. Diagnosis is commonly made after chance findings from screening tests (urinary dipstick or blood tests), or when symptoms become severe. The best available indicator of overall kidney function is GFR, which is measured either via exogenous markers (eg, DTPA, iohexol), or estimated using equations. Presence of proteinuria is associated with increased risk of progression of CKD and death. Kidney biopsy samples can show definitive evidence of CKD, through common changes such as glomerular sclerosis, tubular atrophy, and interstitial fibrosis. Complications include anaemia due to reduced production of erythropoietin by the kidney; reduced red blood cell survival and iron deficiency; and mineral bone disease caused by disturbed vitamin D, calcium, and phosphate metabolism. People with CKD are five to ten times more likely to die prematurely than they are to progress to end stage kidney disease. This increased risk of death rises exponentially as kidney function worsens and is largely attributable to death from cardiovascular disease, although cancer incidence and mortality are also increased. Health-related quality of life is substantially lower for people with CKD than for the general population, and falls as GFR declines. Interventions targeting specific symptoms, or aimed at supporting educational or lifestyle considerations, make a positive difference to people living with CKD. Inequity in access to services for this disease disproportionally affects disadvantaged populations, and health service provision to incentivise early intervention over provision of care only for advanced CKD is still evolving in many countries.

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Chronic hypoxia and tubulointerstitial injury: a final common pathway to end-stage renal failure.

Masaomi Nangaku (2006)

Recent studies emphasize the role of chronic hypoxia in the tubulointerstitium as a final common pathway to end-stage renal failure. When advanced, tubulointerstitial damage is associated with the loss of peritubular capillaries. Associated interstitial fibrosis impairs oxygen diffusion and supply to tubular and interstitial cells. Hypoxia of tubular cells leads to apoptosis or epithelial-mesenchymal transdifferentiation. This in turn exacerbates fibrosis of the kidney and subsequent chronic hypoxia, setting in train a vicious cycle whose end point is ESRD. A number of mechanisms that induce tubulointerstitial hypoxia at an early stage have been identified. Glomerular injury and vasoconstriction of efferent arterioles as a result of imbalances in vasoactive substances decrease postglomerular peritubular capillary blood flow. Angiotensin II not only constricts efferent arterioles but, via its induction of oxidative stress, also hampers the efficient utilization of oxygen in tubular cells. Relative hypoxia in the kidney also results from increased metabolic demand in tubular cells. Furthermore, renal anemia hinders oxygen delivery. These factors can affect the kidney before the appearance of significant pathologic changes in the vasculature and predispose the kidney to tubulointerstitial injury. Therapeutic approaches that target the chronic hypoxia should prove effective against a broad range of renal diseases. Current modalities include the improvement of anemia with erythropoietin, the preservation of peritubular capillary blood flow by blockade of the renin-angiotensin system, and the use of antioxidants. Recent studies have elucidated the mechanism of hypoxia-induced transcription, namely that prolyl hydroxylase regulates hypoxia-inducible factor. This has given hope for the development of novel therapeutic approaches against this final common pathway.

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Renal ischemic injury results in permanent damage to peritubular capillaries and influences long-term function.

David P. J. Osborn, K Roethe, David P Basile … (2001)

Acute episodes of severe renal ischemia result in acute renal failure (ARF). These episodes are followed by a characteristic recovery and repair response, whereby tubular morphology and renal function appear completely restored within approximately 1 mo. However, the chronic effects of such an injury have not been well studied. Male rats were subjected to 60-min bilateral ischemia followed by reperfusion, yielding a characteristic injury. Postischemic animals manifested severe diuresis, peaking at 1 wk postinjury (volume: >45 ml/day, ARF vs. 18 ml/day, sham; P < 0.05). Urine flow subsequently declined but remained significantly elevated vs. sham animals for a 40-wk period. The prolonged alteration in urinary concentrating ability was attributable, in part, to a diminished capacity to generate a hypertonic medullary interstitium. By week 16, proteinuria developed in the post-ARF group and progressed for the duration of the study. Histological examination revealed essentially normal tubular morphology at 4 and 8 wk postinjury but the development of tubulointerstitial fibrosis at 40 wk. Transforming growth factor (TGF)-beta1 expression was elevated at 40 wk, but not at 4 and 8 wk postinjury. Microfil analysis revealed an approximately 30-50% reduction in peritubular capillary density in the inner stripe of the outer medulla at 4, 8, and 40 wk in post-ARF groups vs. sham animals. In addition, post-ARF rats manifested a significant pressor response to a low dose of ANG II (15 ng x kg(-1) x min(-1)). We hypothesize that severe ischemic injury results in a permanent alteration of renal capillary density, contributing to a urinary concentrating defect and the predisposition toward the development of renal fibrosis.