Severe obesity and the impact of medical weight loss on estimated glomerular filtration rate

Rothberg, Amy E.; McEwen, Laura N.; Herman, William H.

doi:10.1371/journal.pone.0228984

Cited by 18 publications

(20 citation statements)

References 18 publications

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“…Our results show that, despite the absence of type 2 diabetes, using EPI formula with non‐indexed GFR, HF is present in a large percentage of cases (35%). This is in keeping with other studies showing that subjects with severe obesity have higher measured creatinine clearance and eGFR than people of normal weight 24,25 . In fact, in severe obesity, BMI reflects not only a disproportionate amount of fat mass, but also an increase in lean mass, which is known to provide the greatest contribution to the circulating levels of creatinine 22 .…”

Section: Discussionsupporting

confidence: 91%

“…showing that subjects with severe obesity have higher measured creatinine clearance and eGFR than people of normal weight. 24,25 In fact, in severe obesity, BMI reflects not only a disproportionate amount of fat mass, but also an increase in lean mass, which is known to provide the greatest contribution to the circulating levels of creatinine. 22 Our study shows a strong association between lean mass and risk of HF, similarly to previous reports in morbidly obese patients.…”

Section: Discussionmentioning

confidence: 99%

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Glomerular hyperfiltration in morbid obesity: Role of the inflammasome signalling

et al. 2022

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Aim Obesity is associated with glomerular hyperfiltration which may precede the development of overt renal damage. Few studies evaluated the link between inflammasome signalling and hyperfiltration. The aim is to evaluate the relationship between IL1‐β/Caspase‐1, insulin sensitivity and hyperfiltration in subjects with severe obesity, before and after weight loss. Methods Forty‐six patients with BMI > 35 kg/m2, without type‐2‐diabetes or hypertension, were evaluated at baseline and 6 months after bariatric surgery with oral glucose tollerance test, bioimpedance analysis and blood tests. The eGFR was calculated according to EPIcr‐cys formula and insulin sensitivity by Oral Glucose Insulin Sensitivity. IL‐1β/Caspase‐1 were measured with the ELISA‐kit. HF was defined as eGFR ≥ 140 ml/min (non‐indexed for BSA). Results Sixteen subjects at baseline had hyperfiltration, with a higher insulin resistance, BMI, lean mass and plasma levels of IL‐1β/Caspase‐1. After surgery, there was a reduction in BMI and improvement in insulin resistance in all patients. However, in 8 of 16 patients hyperfiltration persisted and IL‐1β/Caspase‐1 levels did not decrease (3.22 ± 0.79 vs. 3.13 ± 1.03 and 23.7 ± 12.1 vs. 20.6 ± 9.1, pre vs. post, pg/ml), while cytokines normalized in all the other patients in parallel with the eGFR. In a logistic regression model, correcting for the main covariates, lean mass and IL‐1β before surgery (p = .01 and p = .03, respectively), were the only predictors of hyperfiltration. Conclusion Weight loss is effective in reducing hyperfiltration in most, but not all patients. Hyperfiltration remains unchanged in subjects who do not have a reduction in IL‐1β/Caspase‐1, suggesting a pathogenetic role of the inflammasome signalling in the early stages of nephropathy.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Glomerular hyperfiltration in morbid obesity: Role of the inflammasome signalling

et al. 2022

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“…In contrast, cystatin C synthesis has been shown to be upregulated in adipose tissue in obese individuals and to counteract inflammation of peripheral insulin-sensitive tissues [ 41 ]. Recently it has been shown that in severely obese subjects enrolled in medical weight loss programmes, cystatin C–based eGFR and indexation to actual body surface area (BSA) instead of 1.73 m 2 may provide the most accurate estimate of kidney function [ 42 ]. Also, Chang et al [ 43 ] assessed kidney function before and after bariatric surgery and observed a decrease in absolute iohexol clearance, while the creatinine-based eGFR overestimated and the cystatin C-based eGFR underestimated mGFR.…”

Section: Effect Of Body Compositionmentioning

confidence: 99%

Assessment of kidney function: clinical indications for measured GFR

Ebert

Bevc

Bökenkamp

et al. 2021

Clinical Kidney Journal

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In the vast majority of cases, glomerular filtration rate (GFR) is estimated using serum creatinine, which is highly influenced by age, sex, muscle mass, body composition, severe chronic illness and many other factors. This often leads to misclassification of patients or potentially puts patients at risk for inappropriate clinical decisions. Possible solutions are the use of cystatin C as an alternative endogenous marker or performing direct measurement of GFR using an exogenous marker such as iohexol. The purpose of this review is to highlight clinical scenarios and conditions such as extreme body composition, black race, disagreement between creatinine- and cystatin C-based estimated GFR (eGFR), drug dosing, liver cirrhosis, advanced chronic kidney disease and the transition to kidney replacement therapy, non-kidney solid organ transplant recipients, and living kidney donors where creatinine-based GFR estimation may be invalid. In contrast to the majority of literature on measured GFR (mGFR), this review does not include aspects of mGFR for research or public health settings but aims to reach practicing clinicians and raise their understanding of the substantial limitations of creatinine. While including cystatin C as a renal biomarker in GFR estimating equations has been shown to increase the accuracy of the GFR estimate, there are also limitations to eGFR based on cystatin C alone or the combination of creatinine and cystatin C in the clinical scenarios described above that can be overcome by measuring GFR with an exogenous marker. We acknowledge that mGFR is not readily available in many centres but hope that this review will highlight and promote the expansion of kidney function diagnostics using standardized mGFR procedures as an important milestone towards more accurate and personalized medicine.

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“…В нашем исследовании было подтверждено, что у больных неосложненной ГБ без ХБП при увеличении цистатина С до 1016 нг/мл и выше и снижении СКФ (CKD-EPIcys) до 74 мл/мин/1,73 м 2 и ниже наличие НТГ, ДД ЛЖ, ГЛЖ и увеличения ИОЛП не только дополнительно увеличивают риск развития ХСН, но могут быть самостоятельными маркерами увеличения цистатина С и снижения СКФ. Так, в исследовании Rothberg AE, et al (2020) у больных с тяжелым ожирением, которые снижали массу тела на величину до 18% от исходной, было найдено, что по мере уменьшения гиперинсулинемии с высокой частотой регистрировалась гиперфильтрация (рСКФ ≥135 мл/мин), оцененная по СКФ, основанной в большей степени на определении цистатина С [19]. В одном из экспериментальных исследований было найдено, что НТГ также связано и с канальцевой дисфункцией [20].…”

Section: Discussionunclassified

Risk of heart failure depending on the state of renal filtration function in patients with uncomplicated hypertension

Chernyavina

Козиолова

2022

Russ J Cardiol

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Aim. To assess the risk of heart failure (HF) depending on the state of renal filtration function in patients with uncomplicated hypertension (HTN) without kidney dysfunction.Material and methods. This cross-sectional screening clinical trial consecutively included 176 outpatients with uncomplicated HTN and without chronic kidney disease (CKD). To assess the HF risk, the blood concentration of N-terminal pro-brain natriuretic peptide (NT-proBNP) was determined. To assess the renal filtration function, the blood serum concentration of creatinine and cystatin C was determined, followed by glomerular filtration rate (GFR) estimation using the CKDEPI equation with both parameters. Echocardiography was performed to assess the cardiac structural and functional state.Results. Correlation analysis revealed a moderate direct relationship between NT-proBNP and blood cystatin C concentration (r=0,370; p<0,005), as well as a moderate inverse relationship with GFR (CKD-EPIcre) and GFR (CKD-EPIcys) (r= -0,321; p<0,05 and r=-0,360; p<0,005, respectively). ROC curve for all available values of blood cystatin C revealed the most optimal cut-off threshold of 1016 ng/ml (AUC=0,726, p<0,001), which ensures the sensitivity of 72,2% (p<0,001) and specificity of 62,0% (p<0,001). ROC curve for all available GFR values (CKD-EPIcys) revealed a cut-off threshold of 74 ml/min/1,73 m2 (AUC=0,702, p=0,002) with a sensitivity and specificity of 55,6% and 74,7%, respectively (p=0,001 and p=0,001, respectively). Taking into account the cut-off points for cystatin C and GFRcys, the first group consisted of 73 (41,48%) patients with cystatin C ≥1016 ng/ml and GFR (CKD-EPIcys) ≤74 ml/min/1,73 m2, while the second one — 103 (58,52%) patients with cystatin C <1016 pg/ml and GFR (CKDEPIcys) >74 ml/min/1,73 m2. The presence of impaired glucose tolerance, left ventricular diastolic dysfunction (LV DD), LV hypertrophy and left atrial enlargement leads to an additional increase in HF risk in patients with uncomplicated HNT without CKD.Conclusion. The ROC analysis showed that cystatin C and cystatin C-based GFR (CKD-EPIcys) can be used as markers of HF risk in patients with uncomplicated HTN without CKD. With an increase in cystatin C ≥1016 ng/ml, the relative risk of HF is 2,99, while with a decrease in GFR (CKD-EPIcys) ≤74 ml/min/1,73 m2 — 1,26. The presence of impaired glucose tolerance, LV DD, LV hypertrophy and left atrial enlargement in patients with uncomplicated HTN without CKD with a cystatin C increase ≥1016 ng/ml and a decrease in GFR (CKD-EPIcys) ≤74 ml/min/1,73 m2 and below further increases the risk of developing CHF.

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Severe obesity and the impact of medical weight loss on estimated glomerular filtration rate

Cited by 18 publications

References 18 publications

Glomerular hyperfiltration in morbid obesity: Role of the inflammasome signalling

Glomerular hyperfiltration in morbid obesity: Role of the inflammasome signalling

Assessment of kidney function: clinical indications for measured GFR

Risk of heart failure depending on the state of renal filtration function in patients with uncomplicated hypertension

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