Journal watch
Study Library
Every entry is bound to a primary source, carries an evidence tier, and reports effect sizes with confidence intervals. Paraphrased summaries, plain enough to brief a colleague in a sentence. Grouped into four sections: practice-defining evidence & guidelines; obesity-therapy trials & emerging agents; transplant, dialysis & special populations; and foundations (mechanism, diagnosis & safety).
Last updated: September 2, 2026
Practice-defining evidence & guidelines
Semaglutide slows kidney disease in type 2 diabetes (FLOW)
Weekly semaglutide reduced major kidney events by 24% (HR 0.76, 95% CI 0.66–0.88) in adults with type 2 diabetes and CKD; the trial stopped early for efficacy. Bottom line: In type 2 diabetes with CKD, weekly semaglutide cut major kidney events by about 24% — GLP-1 therapy now has dedicated kidney-outcome evidence.PubMed ↗ · DOI ↗
Kidney outcomes with semaglutide in obesity without diabetes (SELECT)
In adults with obesity and cardiovascular disease but no diabetes, the composite kidney endpoint was lower with semaglutide (HR 0.78, 95% CI 0.63–0.96). A prespecified secondary kidney analysis within a cardiovascular-outcomes trial — not a dedicated kidney-outcome trial. Bottom line: Even without diabetes, semaglutide lowered a composite kidney endpoint in obesity with cardiovascular disease — a secondary signal, not a dedicated kidney trial.PubMed ↗ · DOI ↗ · Free full text ↗
Finerenone, a non-steroidal MRA, in diabetic CKD (FIDELITY)
Across the FIDELIO-DKD and FIGARO-DKD program, the non-steroidal mineralocorticoid-receptor antagonist finerenone reduced kidney and cardiovascular events in type 2 diabetes with CKD — the fourth pillar of cardio-renal-metabolic protection. Bottom line: Finerenone adds kidney and cardiovascular protection on top of RAS blockade in diabetic CKD — the nonsteroidal MRA “fourth pillar.”PubMed ↗ · DOI ↗ · Free full text ↗
First multisociety CKM syndrome guideline
The first comprehensive clinical practice guideline for cardiovascular-kidney-metabolic syndrome (2026 AHA/ACC/ADA/ASN guideline), building on the AHA 2023 Presidential Advisory and its staging system (stages 0 through 4) of the CKM continuum. Bottom line: The first multisociety framework to stage and manage cardiovascular-kidney-metabolic disease as one connected syndrome.PubMed ↗ · DOI ↗ · Free full text ↗
Obesity and CKD: KDIGO Controversies Conference (Prague 2024)
Conclusions from the KDIGO conference on the pathophysiology, prognosis, and management of obesity in CKD — with long-duration, early-onset obesity carrying the highest risk of incident CKD. Bottom line: Consensus that obesity is a modifiable driver of CKD, calling for stigma-free, multidisciplinary management.PubMed ↗ · DOI ↗ · Free full text ↗
KDIGO 2024 clinical practice guideline for CKD
The updated CKD guideline, including use of the combined creatinine–cystatin C eGFR equation when creatinine alone is unreliable. Bottom line: The current global standard for diagnosing, risk-staging, and treating CKD, including SGLT2 inhibitors.PubMed ↗ · DOI ↗ · Free full text ↗
ASN Kidney Health Guidance on obesity in kidney disease
The ASN first guidance on managing obesity in people with kidney disease — spanning psychosocial care, lifestyle, pharmacotherapy, and metabolic/bariatric surgery within a multidisciplinary team. Bottom line: Practical nephrology guidance on assessing and treating obesity in kidney disease, including GLP-1 use and dosing.PubMed ↗ · DOI ↗ · Free full text ↗
KDOQI clinical practice guideline for nutrition in CKD (2020 update)
The KDOQI nutrition guideline for CKD: protein targets across CKD stages and dialysis — including higher protein needs on maintenance dialysis — the framework for reconciling weight-loss goals with protein and muscle preservation. Bottom line: The reference for protein and nutrition targets across CKD stages and dialysis.PubMed ↗ · DOI ↗ · Free full text ↗
Obesity-therapy trials & emerging agents
Semaglutide in metabolic dysfunction-associated steatohepatitis (ESSENCE)
At 72 weeks (planned interim analysis), resolution of steatohepatitis without worsening fibrosis occurred in 62.9% on semaglutide vs 34.3% on placebo. Liver (MASH) outcome evidence within the CKM continuum, not a kidney-outcome trial. Bottom line: Semaglutide resolved steatohepatitis without worsening fibrosis in 62.9% vs 34.3% on placebo — extending GLP-1 benefit to MASH.PubMed ↗ · DOI ↗
Tirzepatide in HFpEF with obesity (SUMMIT)
The dual GIP/GLP-1 agonist tirzepatide improved heart-failure outcomes and symptoms in HFpEF with obesity — a single positive trial on a cardiac endpoint, included here as it extends the CKM story to the heart; renal outcomes were secondary/exploratory, not a primary endpoint. Bottom line: Tirzepatide improved outcomes and symptoms in HFpEF with obesity — extending the CKM story to the heart (renal endpoints exploratory).PubMed ↗ · DOI ↗
Cardiovascular outcomes: tirzepatide vs dulaglutide (SURPASS-CVOT)
In type 2 diabetes at high cardiovascular risk, tirzepatide was noninferior to dulaglutide — an active GLP-1 comparator, not placebo — for major adverse cardiovascular events. A cardiovascular-safety benchmark against an active drug; a dedicated hard kidney-outcome result is not its primary finding. Bottom line: Tirzepatide was noninferior to dulaglutide for major cardiovascular events — an active-comparator safety benchmark, not a kidney trial.PubMed ↗ · DOI ↗
Retatrutide, a triple agonist: early kidney signals
Phase-2 post-hoc analyses showed reductions in urine albumin-to-creatinine ratio. The phase-2b TRANSCEND-CKD study (renal function by iohexol mGFR) reached primary completion in late 2025, with results emerging; the pivotal TRIUMPH-Outcomes program is not expected before 2028–2029. No phase-3 kidney endpoints yet. Bottom line: The triple GIP/GLP-1/glucagon agonist produced large early weight loss with favorable metabolic signals — early phase, kidney data preliminary.PubMed ↗ · DOI ↗
Tirzepatide once weekly for obesity (SURMOUNT-1)
In adults with obesity without diabetes, tirzepatide produced dose-dependent mean weight reductions up to roughly 21% at the highest dose over 72 weeks — the landmark dual-agonist obesity trial. Bottom line: Tirzepatide delivered the largest weight loss yet seen with a medication in obesity without diabetes.PubMed ↗ · DOI ↗
Tirzepatide kidney outcomes (SURPASS-4, post-hoc)
A post-hoc analysis of SURPASS-4 (tirzepatide vs insulin glargine in T2D at high CV risk) found a lower composite kidney endpoint with tirzepatide (HR 0.58, 95% CI 0.43–0.80), driven largely by reduced albuminuria. Exploratory, not a dedicated kidney-outcome trial. Bottom line: Post hoc, tirzepatide slowed eGFR decline and albuminuria versus insulin glargine — hypothesis-generating, not a primary kidney endpoint.PubMed ↗ · DOI ↗
Tirzepatide vs dulaglutide: major kidney events (SURPASS-CVOT)
A prespecified exploratory kidney analysis of SURPASS-CVOT found fewer major kidney events with tirzepatide than with dulaglutide (HR 0.77, 95% CI 0.68–0.88; 6.0% vs 7.6%), and a slower annual eGFR decline (by 0.29 mL/min/1.73 m² overall, 0.93 in those at high kidney risk). The comparator was an active GLP-1 agent, not placebo, and the benefit was driven mainly by less new persistent macroalbuminuria. Bottom line: The strongest kidney-event signal for tirzepatide to date — but exploratory, against an active comparator, and albuminuria-driven; a dedicated placebo-controlled kidney-outcome trial is still missing.PubMed ↗ · DOI ↗
Kidney parameters with tirzepatide in obesity (SURMOUNT-1 / SURMOUNT-2)
Post hoc analysis of the two pivotal obesity trials. Placebo-corrected UACR at week 72 was −8.4% (95% CI −14.7 to −1.6) in obesity without diabetes and −31.1% (95% CI −40.9 to −19.7) in obesity with type 2 diabetes. The effect concentrated in participants who already had albuminuria at baseline (UACR ≥30 mg/g): −42.3% (95% CI −60.8 to −15.0) and −55.2% (95% CI −68.5 to −36.4) respectively. In SURMOUNT-1, cystatin C–based eGFR rose versus placebo (+3.2 mL/min/1.73 m², 95% CI 2.1 to 4.3; combined creatinine–cystatin C +1.9 mL/min/1.73 m², 95% CI 0.9 to 2.9); in SURMOUNT-2 both groups rose with no between-group difference. Biomarker endpoints in a post hoc analysis, not a kidney-outcome trial. Bottom line: Tirzepatide lowered albuminuria in obesity with and without diabetes, with by far the largest effect where albuminuria was already present.PubMed ↗ · DOI ↗
Once-weekly semaglutide 2.4 mg for obesity (STEP 1)
In adults with obesity without diabetes, once-weekly semaglutide 2.4 mg produced a mean weight change of about −15% versus roughly −2.4% with placebo over 68 weeks — the landmark obesity-efficacy trial for semaglutide. Bottom line: Semaglutide 2.4 mg produced substantial weight loss in obesity without diabetes — the trial that opened the modern GLP-1 era.PubMed ↗ · DOI ↗
Transplant, dialysis & special populations
GLP-1 receptor agonists in kidney transplant recipients
A systematic review and meta-analysis (n ≈ 240) found weight loss of about 4 kg and an HbA1c reduction near 0.85% with GLP-1 RAs in kidney transplant recipients, alongside stable eGFR and reduced albuminuria. Tacrolimus levels remained stable and no rejection signal was reported — observational, but consistent and reassuring. Bottom line: GLP-1 receptor agonists appear effective and generally well tolerated in kidney transplant recipients — mind drug interactions and volume status.PubMed ↗ · DOI ↗ · Free full text ↗
Bariatric surgery and kidney transplant access
Pre-transplant weight-loss surgery is associated with higher rates of subsequent waitlisting and transplantation in patients with obesity and kidney failure, without a signal of worse graft outcomes — supporting bariatric surgery as a bridge to candidacy. Bottom line: Pre-transplant weight-loss surgery is linked to more waitlisting and transplantation without worse graft outcomes — supporting surgery as a bridge to candidacy.PubMed ↗ · DOI ↗ · Free full text ↗
The obesity paradox in dialysis (reverse epidemiology)
In maintenance hemodialysis, higher BMI is repeatedly associated with lower mortality — largely reflecting preserved muscle mass and nutritional reserve rather than protective adiposity. Cautions against reflexive weight-loss targets on dialysis. Bottom line: On hemodialysis, higher BMI tracks with lower mortality — largely muscle and nutritional reserve, so avoid reflexive weight-loss targets.PubMed ↗ · DOI ↗ · Free full text ↗
PD glucose load, body composition, and icodextrin
Glucose absorption from conventional peritoneal dialysate is associated with a gain in fat mass and a loss of lean mass; glucose-sparing icodextrin for the long dwell attenuates fat accumulation and aids volume control. Bottom line: Glucose absorbed from peritoneal dialysate promotes fat gain and lean-mass loss; icodextrin for the long dwell limits this and aids volume control.PubMed ↗ · DOI ↗
Bariatric surgery vs intensive medical therapy, 5-year outcomes (STAMPEDE)
At five years, bariatric surgery (sleeve gastrectomy or gastric bypass) achieved superior glycemic control versus intensive medical therapy in type 2 diabetes — foundational evidence for the durable metabolic effect of metabolic surgery. Bottom line: At five years, metabolic surgery beat intensive medical therapy for glycemic control in type 2 diabetes — a durable metabolic effect.PubMed ↗ · DOI ↗ · Free full text ↗
APOL1 risk variants and CKD progression (AASK/CRIC)
In Black participants of the AASK and CRIC cohorts, APOL1 high-risk genotypes were associated with faster progression of chronic kidney disease — the basis for APOL1 as a gene–environment risk modifier relevant to this population. Bottom line: APOL1 high-risk genotypes accelerate CKD progression in people of West African ancestry — a key gene-environment risk modifier.PubMed ↗ · DOI ↗ · Free full text ↗
Foundations: mechanism, diagnosis & safety
Euglycemic DKA with SGLT2 inhibitors (2024 multisociety consensus)
The hyperglycemic-crises consensus report covering the recognition and management of euglycemic ketoacidosis — a key renal-safety consideration. Bottom line: A consensus on recognizing and managing SGLT2 inhibitor-associated euglycemic ketoacidosis — a practical kidney-safety must-know.PubMed ↗ · DOI ↗ · Free full text ↗
Race-free GFR equations, including combined creatinine–cystatin C (CKD-EPI 2021)
New creatinine, cystatin C, and combined creatinine–cystatin C equations that estimate GFR without a race coefficient; the combined equation is more accurate than either marker alone — the basis for confirming GFR when creatinine is unreliable, as in changing muscle mass. Bottom line: Race-free GFR equations; the combined creatinine-cystatin C formula is most accurate — use it to confirm GFR when creatinine is unreliable.PubMed ↗ · DOI ↗ · Free full text ↗
Measuring GFR before and after bariatric surgery
Pooled data from all seven available studies (2004–2018) that measured GFR before and after bariatric surgery by gold-standard methods: 105 individuals from the United States and Europe, 68% female, mean age 50 years (range 24–70), mean BMI 46 ± 8 kg/m². Mean measured GFR fell from 107 mL/min (range 31–215) to 92 mL/min, a 14% decline (95% CI −21 to −10), with larger falls in those starting from a higher GFR. Correlation with the amount of weight lost was weak. GFR-estimating equations performed better when deindexed and when applied in people with reduced kidney function, and the combined creatinine–cystatin C equations performed best overall. Bottom line: GFR falls about 14% after bariatric surgery — largely the reversal of hyperfiltration, not injury — and the deindexed combined creatinine–cystatin C equation tracks it most reliably.PubMed ↗ · DOI ↗
Obesity-related glomerulopathy: the defining description (Kambham)
The landmark clinicopathologic description of ORG: glomerulomegaly with or without a perihilar focal segmental lesion, often heavy but sub-nephrotic proteinuria with milder foot-process effacement than primary FSGS, and a rising incidence — the histologic basis for treating ORG as its own entity. Bottom line: The paper that defined obesity-related glomerulopathy (glomerulomegaly with or without FSGS, rising incidence) — the histologic foundation of the field.PubMed ↗ · DOI ↗
Weight loss and proteinuria in obesity-related glomerulopathy
63 patients with biopsy-proven obesity-related glomerulopathy entered a physician-supervised diet-and-exercise programme and were grouped by weight change over two years. At six months, 27 patients had lost 8.29 ± 4.00% and mean proteinuria had fallen by 35.3%; at 24 months, 27 patients reached a 9.20 ± 3.78% BMI reduction with a 51.33% fall in urine protein excretion. In those whose BMI rose, urine protein increased by 28.78%. On multivariate regression, change in BMI was the only predictor of change in proteinuria (P < 0.01). Single-centre cohort, not randomised, no comparison against pharmacotherapy. Bottom line: In biopsy-proven ORG, a roughly 8–9% weight reduction cut proteinuria by a third at six months and by half at two years — and weight regain reversed the gain.PubMed ↗ · DOI ↗ · Free full text ↗