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Kidney function and markers of renal damage after renal denervation. Does method of measurement matter? The Reshape CV-Risk Study.

ABSTRACT: Data suggest that renal denervation (RDN) in treatment-resistant hypertension (TRHT) is safe in terms of renal function. However, most studies report kidney function as creatinine-based estimated glomerular filtration rate (eGFR), which may be biased by non-renal factors. Damage markers other than albuminuria have never been evaluated after RDN. In this non-randomized RDN trial, we studied changes in kidney function, assessed as measured GFR (mGFR) and various GFR estimates, six months and two years after RDN. We also examined changes in albuminuria and a biomarker of tubular dysfunction. Adult non-diabetic patients with TRHT and eGFR ≥45 ml/min/1.73 m² were recruited from hypertension clinics. Before bilateral RDN, mGFR was measured by iohexol clearance. We estimated eGFR from serum creatinine and cystatin C (eGFR_crea , eGFR_cys, and eGFR_creacys ), and albumin-creatinine ratio (ACR) and N-acetyl-β-D-glucosaminidase (NAG)-creatinine ratio (NAG-CR) were measured in spot urines. All measurements were repeated after six and twenty-four months. Twenty patients, mean age 54 (±9) years and baseline mGFR 83 (±20) ml/min/1.73 m² underwent RDN. After six months, mGFR fell, eGFR_crea remained unchanged, whereas eGFR_cys and eGFR_creacys increased. At 2 years' follow-up, eGFR_creacys was significantly lower than at baseline. mGFR was 78 (±28) ml/min/1.73 m² . Change in ambulatory systolic BP predicted change in eGFR_crea . Urinary NAG-CR, but not ACR, increased during follow-up. Different GFR assessments gave diverging results after RDN. Therefore, care should be taken to method when evaluating kidney function after RDN. Increases in a tubular dysfunction biomarker suggest that kidney damage may occur. Long-term renal follow-up is needed after RDN.

SUBMITTER: Solbu MD

PROVIDER: S-EPMC8678667 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND:Central aortic blood pressures and arterial stiffness are better indicators of cardiovascular outcomes than brachial blood pressures. However, their response to renal denervation (RDN) in patients with stage 3 and stage 4 chronic kidney disease (CKD) has not yet been examined. OBJECTIVE:To evaluate the impact of RDN on central blood pressures, brachial (office and ambulatory) blood pressures, arterial stiffness, glomerular filtration rate (GFR), 24-hour urine protein, and selective cardiac parameters observed on echocardiograms. DESIGN:Single-center, single-arm with pre-RDN/post-RDN follow-up. SETTING:Patients are being recruited from the multidisciplinary CKD clinic. PATIENTS:Fifty consecutive patients with stage 3 or stage 4 CKD and resistant hypertension, with no radiological or laboratory evidence of secondary causes of hypertension. MEASUREMENTS:The key measurements are central blood pressures, pulse wave velocity, ambulatory 24-hour blood pressure, office blood pressures on BP Tru, GFR, 24-hour urine protein and sodium, blood pressure medication, and doses. METHODS:For our primary outcome, we will compare changes in central blood pressures from baseline to 6 months post RDN using a paired t test or Mann-Whitney U test. Secondary outcomes will examine changes in central blood pressures from baseline to 3, 12, 18, and 24 months post RDN as well as changes in office pressures, GFR, 24-hour urine protein and sodium, and medications at all time points using mixed-model analyses of variance or Friedman test. Multiple regression may be used to control for potential covariates. LIMITATIONS:Single-center study, with no sham arm. CONCLUSIONS:Aortic blood pressure, rather than brachial blood pressure, optimally reflects the load placed on the left ventricle. Aortic blood pressure is also better associated with cardiovascular outcomes. If our study shows a preferential decrease in central blood pressures and improvements in cardiac parameters on echocardiograms post RDN, this may influence the way in which blood pressures are managed in clinics and offices. TRIAL REGISTRATION:ClinicalTrials.gov (NCT01832233).

Project description:Under specific conditions non-steroidal anti-inflammatory drugs (NSAIDs) may be used to lower therapy-resistant proteinuria. The potentially beneficial anti-proteinuric, tubulo-protective, and anti-inflammatory effects of NSAIDs may be offset by an increased risk of (renal) side effects. We investigated the effect of indomethacin on urinary markers of glomerular and tubular damage and renal inflammation. We performed a post-hoc analysis of a prospective open-label crossover study in chronic kidney disease patients (n = 12) with mild renal function impairment and stable residual proteinuria of 4.7±4.1 g/d. After a wash-out period of six wks without any RAAS blocking agents or other therapy to lower proteinuria (untreated proteinuria (UP)), patients subsequently received indomethacin 75 mg BID for 4 wks (NSAID). Healthy subjects (n = 10) screened for kidney donation served as controls. Urine and plasma levels of total IgG, IgG4, KIM-1, beta-2-microglobulin, H-FABP, MCP-1 and NGAL were determined using ELISA. Following NSAID treatment, 24 h -urinary excretion of glomerular and proximal tubular damage markers was reduced in comparison with the period without anti-proteinuric treatment (total IgG: UP 131[38-513] vs NSAID 38[17-218] mg/24 h, p<0.01; IgG4: 50[16-68] vs 10[1-38] mg/24 h, p<0.001; beta-2-microglobulin: 200[55-404] vs 50[28-110] ug/24 h, p = 0.03; KIM-1: 9[5]-[14] vs 5[2]-[9] ug/24 h, p = 0.01). Fractional excretions of these damage markers were also reduced by NSAID. The distal tubular marker H-FABP showed a trend to reduction following NSAID treatment. Surprisingly, NSAID treatment did not reduce urinary excretion of the inflammation markers MCP-1 and NGAL, but did reduce plasma MCP-1 levels, resulting in an increased fractional MCP-1 excretion. In conclusion, the anti-proteinuric effect of indomethacin is associated with reduced urinary excretion of glomerular and tubular damage markers, but not with reduced excretion of renal inflammation markers. Future studies should address whether the short term glomerulo- and tubulo-protective effects as observed outweigh the possible side-effects of NSAID treatment on the long term.

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Kidney function and markers of renal damage after renal denervation. Does method of measurement matter? The Reshape CV-Risk Study.

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