# Left Ventricular Mass Index Predicts Renal Function Decline in Patients with Chronic Kidney Disease

**Authors:** Antonio Lacquaniti, Fabrizio Ceresa, Susanna Campo, Francesco Patané, Paolo Monardo

PMC · DOI: 10.3390/medicina60010127 · 2024-01-10

## TL;DR

This study shows that higher left ventricular mass index in patients with chronic kidney disease is linked to faster kidney function decline.

## Contribution

The study identifies left ventricular mass index as an independent predictor of renal function decline in CKD patients.

## Key findings

- Patients with CKD and higher LVMi had a 12% increased risk of kidney disease progression.
- LVMi remained a significant predictor after adjusting for kidney and cardiac risk factors.
- Echocardiography can identify high-risk CKD patients independently of clinical cardiac involvement.

## Abstract

Background and Objectives: Several studies revealed a relation between abnormal cardiac remodeling and glomerular filtration rate (GFR) decline, but there are limited data regarding echocardiographic changes in chronic kidney disease (CKD). This study evaluated the abnormal cardiac structures characterizing patients with CKD, assessing the independent association between echocardiographic parameters and the risk of decline in renal function. Materials and Methods: In total, 160 patients with CKD were studied. All patients underwent an echocardiographic exam and 99mTc-DTPA renal scintigraphy to measure the GFR. After the baseline assessments, patients were followed prospectively for 12 months, or until the endpoint achievement, defined as a worsening in renal function (doubling of baseline serum creatinine, GFR decline ≥25%, the start of dialysis). Results: Patients with GFR values of 34.8 ± 15 mL/min, identifying stages III–IV of CKD, were associated with high levels of left ventricular mass index (LVMi) (101.9 ± 12.2 g/m2), which was related to proteinuria, systolic blood pressure, and pulmonary artery systolic pressure in a multiple regression model. During the observational period, 26% of patients reached the endpoint. Regression analysis revealed LVMi as a predictor of change in renal function after adjusting for kidney and cardiac risk factors. Multiple Cox regression indicated that an increase in LVMi was associated with a 12% increased risk of kidney disease progression (HR: 1.12; 95% CI: 1.04–1.16; p = 0.001). Conclusions: In patients with CKD, high LVMi represents an independent predictor of the progressive decline of the renal function, until the start of renal replacement therapy. Echocardiography can help identify patients at high risk for renal disease worsening in patients with CKD independently of clinical cardiac involvement.

## Linked entities

- **Diseases:** chronic kidney disease (MONDO:0005300), renal disease (MONDO:0005240)

## Full-text entities

- **Genes:** PTH (parathyroid hormone) [NCBI Gene 5741] {aka FIH1, PTH1}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, AGT (angiotensinogen) [NCBI Gene 183] {aka ANHU, SERPINA8, hFLT1}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}
- **Diseases:** endothelial dysfunction (MESH:D014652), CKD (MESH:D051436), renal failure (MESH:D051437), proteinuria (MESH:D011507), coronary artery diseases (MESH:D003324), inflammation (MESH:D007249), pulmonary involvement (MESH:C566343), hypertrophy (MESH:D006984), cardiac and kidney failure (MESH:D006333), myocardial steatosis (MESH:D005234), cardio-renal syndrome (MESH:D059347), injury to people or property (MESH:C000719191), cardiac (MESH:D006331), vascular calcification (MESH:D061205), kidney disease (MESH:D007674), pulmonary artery hypertension (MESH:D000081029), cardiac fibrosis (MESH:D005355), LV hypertrophy (MESH:D017379), cardiac remodeling (MESH:D020257), anemia (MESH:D000740), cardiac abnormalities (MESH:D018376), LVM (MESH:D018487), hypertension (MESH:D006973), acute kidney injury (MESH:D058186), cardiovascular disease (MESH:D002318), ESRD (MESH:D007676), PH (MESH:D006976), fluid overload (MESH:D019190), diabetic (MESH:D003920), abnormalities (MESH:D000014), calcific arteriosclerosis (MESH:D001161), IgA nephropathy (MESH:D005922), ventricular hypertrophy (MESH:D024741), decline (MESH:D060825)
- **Chemicals:** uric acid (MESH:D014527), sodium (MESH:D012964), aldosterone (MESH:D000450), empagliflozin (MESH:C570240), creatinine (MESH:D003404), 1,25 dihydroxyvitamin D3 (MESH:D002117), water (MESH:D014867), 99mTc-DTPA (-), steroids (MESH:D013256), NPs (MESH:D045265), vitamin D (MESH:D014807), salt (MESH:D012492), monocrotaline (MESH:D016686)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]

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Source: https://tomesphere.com/paper/PMC10820232