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Kidneys

Everything in the library studied for it, medical and holistic together. Within each kind, what was shown to help comes first, strongest evidence first. What was tested and not shown to help stays on the list.

Strong several reviews agree · Moderate one review or consistent trials · Limited one or a few small studies · Untested no study in people, listed with what it rests on

Medication16 Supplements1 Lab markers22

Medication

Alpha-blockersStrongCommon

Passing a ureteral stone

Shown to raise stone passage, about 116 more per 1,000 in placebo-controlled trials, mainly for stones over 5 mm. Stones of 5 mm or less showed no clear benefit.

Compared with placebo or standard therapy [9]; placebo or control [10]

The numbers and sources

How common: Common: between 1 in 100 and 1 in 10 people.
Effect: Across all trials, stone clearance rose on an alpha-blocker (RR 1.45, 95% CI 1.36 to 1.55, low quality). In the higher-quality placebo-controlled trials the effect was smaller (RR 1.16, 95% CI 1.07 to 1.25), or 116 more clearances per 1,000. For stones 5 mm or smaller the RR was 1.06 (95% CI 0.98 to 1.15). Expulsion took 3.40 fewer days and hospital stays were fewer (RR 0.51) [9]. A second meta-analysis found more passage overall (RR 1.49, 95% CI 1.39 to 1.61), no clear benefit for smaller stones (RR 1.19, 95% CI 1.00 to 1.48) and 57% more passage for larger ones (RR 1.57, 95% CI 1.17 to 2.27), with less surgery (RR 0.44) [10].
Population: 10,509 adults in 67 trials, 5,787 of them in 15 placebo trials, with stones 1 cm or smaller [9]; 55 randomized trials [10].
Sources: [9], [10]
Caveats: Many trials were small and at risk of bias, and effects shrank in placebo-controlled trials [9]. Most trials used tamsulosin.

KetoanaloguesStrong

Kidney function decline in chronic kidney disease

Shown to slow kidney function decline in adults with chronic kidney disease when added to a protein-restricted diet. Diet and supplement effects overlap.

The numbers and sources

Effect: In 16 RCTs (1,344 people with stage 3 to 5 CKD, median 13 months), ketoanalogues added to a protein-restricted diet gave a higher GFR than a low-protein diet alone, and a marginally lower risk of kidney failure in people without diabetes [1]. In 17 RCTs (1,459 participants), protein-restricted diets with ketoanalogues preserved eGFR and reduced proteinuria and blood pressure, with a larger eGFR effect on very low-protein diets [2]. In 10 RCTs and 2 non-randomized studies (951 patients), the combination delayed CKD progression (p 0.008), particularly with eGFR above 18 mL/min/1.73 m² [3]. In diabetic kidney disease, a review of 11 studies reported pooled GFR and urinary protein results in favor of ketoanalogues [4]. In non-diabetic adults with eGFR below 30, a ketoanalogue-supplemented vegetarian very low-protein diet for 15 months reduced the composite of starting dialysis or losing half of eGFR (number needed to treat 4.4) against a conventional low-protein diet [5].
Population: Adults with CKD stages 3 to 5 not on dialysis [1][2][3][5]. Adults with diabetic kidney disease not on dialysis [4].
Sources: [1], [2], [3], [4], [5]
Caveats: Many trials paired ketoanalogues with a stricter diet than the control arm, so the effects of diet and supplement overlap [2][5]. Only 14% of screened patients were randomized in [5]. The authors of [1] call for larger, longer trials, especially in diabetes. A Cochrane review of very low-protein diets, with or without ketoanalogues, found 165 fewer people per 1,000 reached kidney failure than on a low-protein diet (RR 0.65, 95% CI 0.49 to 0.85, moderate certainty) [6].

KetoanaloguesStrong

Phosphate and parathyroid hormone

Shown to lower blood phosphate, urea and parathyroid hormone in adults with chronic kidney disease on a protein-restricted diet.

The numbers and sources

Effect: Ketoanalogues added to a protein-restricted diet lowered blood urea nitrogen and phosphorus and raised calcium against a low-protein diet alone [1]. In 17 RCTs, they lowered serum phosphate and parathyroid hormone [2].
Population: Adults with CKD not on dialysis [1][2].
Sources: [1], [2]
Caveats: These are blood markers, not fractures or heart events.

SGLT2 inhibitorsStrongCommon

Kidney disease progression

Shown to cut the risk of kidney disease progression by about 37% in adults with chronic kidney disease, heart failure or type 2 diabetes, with or without diabetes.

The numbers and sources

How common: Common: between 1 in 100 and 1 in 10 people.
Effect: Across 13 trials, allocation to an SGLT2 inhibitor lowered the risk of kidney disease progression by 37% (RR 0.63, 95% CI 0.58 to 0.69), with similar results in people with and without diabetes [4]. In 10 trials, progression occurred at 25.4 against 40.3 events per 1,000 patient-years (HR 0.62, 95% CI 0.57 to 0.68), including at an eGFR below 30 (HR 0.71, 95% CI 0.60 to 0.83), and kidney failure alone fell (HR 0.66, 95% CI 0.58 to 0.75) [5]. With dapagliflozin in chronic kidney disease, the primary kidney and cardiovascular outcome occurred in 9.2% against 14.5% on placebo over a median 2.4 years (HR 0.61, 95% CI 0.51 to 0.72, number needed to treat 19), and death from any cause in 4.7% against 6.8% [6]. With empagliflozin, kidney disease progression or cardiovascular death occurred in 13.1% against 16.9% over a median 2.0 years (HR 0.72, 95% CI 0.64 to 0.82) [7]. With canagliflozin in type 2 diabetes with kidney disease, the primary outcome occurred at 43.2 against 61.2 per 1,000 patient-years (HR 0.70, 95% CI 0.59 to 0.82), and end-stage kidney disease fell (HR 0.68, 95% CI 0.54 to 0.86) [8].
Population: 90,409 participants in 13 trials [4]; 70,361 participants in 10 trials, mean age 64.8 [5]; 4,304 adults with chronic kidney disease [6]; 6,609 adults with chronic kidney disease [7]; 4,401 adults with type 2 diabetes and albuminuric kidney disease [8].
Sources: [4], [5], [6], [7], [8]
Caveats: The two meta-analyses come from the same consortium and share trials [4][5]. The band above is the number needed to treat of 19 in one dapagliflozin trial [6]. Two of the kidney trials were stopped early [6][8]. The trials did not enroll people on dialysis.

ACE inhibitorsModerate

Slowing kidney disease

Shown to slow kidney function loss in people with diabetic kidney disease and in non-diabetic kidney disease with protein in the urine.

The numbers and sources

Effect: In people with type 1 diabetes and kidney disease, serum creatinine doubled in 25 of 207 on captopril and 43 of 202 on placebo, a 48% reduction in risk. The combined risk of death, dialysis or transplantation fell 50% [11]. In individual data from 11 trials in mostly non-diabetic kidney disease, regimens with an ACE inhibitor lowered end-stage kidney disease (RR 0.69, 95% CI 0.51 to 0.94) and the combination of doubled creatinine or end-stage kidney disease (RR 0.70, 95% CI 0.55 to 0.88), with more benefit at higher urine protein [12]. A Cochrane review of 50 studies in diabetic kidney disease found ACE inhibitors and ARBs had similar benefits on kidney outcomes. Mortality against placebo did not differ significantly (RR 0.91, 95% CI 0.71 to 1.17) [13].
Population: 409 people with type 1 diabetes, urine protein of 500 mg a day or more [11]; 1,860 people without diabetes followed a mean of 2.2 years [12]; 13,215 people with diabetic kidney disease in 50 studies [13].
Sources: [11], [12], [13]
Caveats: The evidence in [11] is for captopril. Results were inconclusive for people with urine protein below 0.5 g a day [12].

Alpha-blockersModerateVery common

Stone fragments after shock wave lithotripsy

Shown to raise clearance of stone fragments after lithotripsy, from 69% to about 80%, in evidence a Cochrane review rated low certainty.

Compared with usual care alone or with placebo [13]

The numbers and sources

How common: Very common: more than 1 in 10 people.
Effect: Stone fragment clearance rose on an alpha-blocker plus usual care (RR 1.16, 95% CI 1.09 to 1.23), from 69.3% to an estimated 80.4%, or 111 more per 1,000. Auxiliary treatments fell from 9.7% to 6.5% (RR 0.67, 95% CI 0.45 to 1.00), major adverse events fell from 25.8% to 15.5% (RR 0.60), and clearance came 3.74 days sooner [13].
Population: 4,793 adults in 40 trials, only 4 of them placebo-controlled, mean stone size 7.1 to 13.2 mm [13].
Sources: [13]
Caveats: Low certainty evidence with high heterogeneity (I² 78%) [13]. Most trials used tamsulosin.

ARBs (angiotensin receptor blockers)Moderate

Kidney disease in type 2 diabetes

Shown to slow kidney disease in type 2 diabetes with protein in the urine, with 16 to 20% fewer people reaching kidney failure, doubled creatinine or death.

The numbers and sources

Effect: Over a mean 3.4 years, losartan lowered the composite of doubled creatinine, end-stage kidney disease or death by 16% against placebo (327 against 359 people). Doubled creatinine fell 25% and end-stage kidney disease 28%, with no effect on death [3]. Over a mean 2.6 years, irbesartan lowered the same composite by 20% against placebo and 23% against amlodipine, and doubled creatinine by 33% against placebo [4]. A Cochrane review of 50 studies found ACE inhibitors and ARBs had similar benefits on kidney outcomes, and ARBs did not lower mortality against placebo (RR 0.99, 95% CI 0.85 to 1.17) [5].
Population: 1,513 people with type 2 diabetes and kidney disease [3]; 1,715 people with high blood pressure and kidney disease from type 2 diabetes [4]; 13,215 people with diabetic kidney disease in 50 studies, 5 comparing ARBs with placebo [5].
Sources: [3], [4], [5]
Caveats: The trial evidence is for losartan and irbesartan. Both trials added the ARB to other blood pressure drugs.

Ezetimibe and fenofibrateModerate

Fenofibrate and fibrates: protein in the urine

Shown to slow the progression of albumin in the urine, by 14% across fibrate trials, with less progression on fenofibrate in its main diabetes trial.

Compared with placebo [9][8]

The numbers and sources

Effect: Fibrates lowered the risk of albuminuria progression by 14% (95% CI 2 to 25) [9]. Fenofibrate was associated with less albuminuria progression in people with type 2 diabetes (p=0.002) [8].
Population: Fibrate trials [9]; 9,795 adults with type 2 diabetes [8].
Sources: [9], [8]
Caveats: Albuminuria is a marker of kidney damage, not kidney failure. Fenofibrate raises creatinine, listed under Risks.

InsulinModerate

Eye, kidney and nerve complications in type 1 diabetes

Shown to cut new eye disease by about 76%, kidney protein leakage by 39% to 54% and nerve damage by 60% with intensive insulin treatment in type 1 diabetes.

The numbers and sources

Effect: In people with type 1 diabetes and no eye disease, intensive insulin treatment lowered the risk of developing retinopathy by 76% (95% CI 62 to 85) against conventional treatment. In people with mild retinopathy it slowed progression by 54% (95% CI 39 to 66). Across both groups it lowered microalbuminuria by 39% (95% CI 21 to 52), albuminuria by 54% (95% CI 19 to 74) and clinical neuropathy by 60% (95% CI 38 to 74) [1]. A Cochrane review of 12 trials found retinopathy developed in 6.2% on intensive control against 23.2% on conventional control (RR 0.27, 95% CI 0.18 to 0.42), nephropathy in 16.3% against 28.4% (RR 0.56, 95% CI 0.46 to 0.68) and neuropathy in 4.9% against 13.9% (RR 0.35, 95% CI 0.23 to 0.53) [2].
Population: 1,441 people with type 1 diabetes, assigned to an insulin pump or three or more daily injections, or to one or two daily injections [1]; 2,230 patients in 12 trials followed for 1 to 6.5 years [2].
Sources: [1], [2]
Caveats: The trials compared more intensive with less intensive insulin treatment. Neither arm went without insulin. The largest trial dominates the review [2]. Once complications were present, the effect was weaker for eye disease and uncertain for kidney disease [2].

AllopurinolLimited

Preventing calcium oxalate kidney stones

One trial found fewer kidney stone events on allopurinol, 0.12 against 0.26 per patient a year, in people with high urinary uric acid.

The numbers and sources

Effect: In people with recurrent calcium oxalate stones, high urinary uric acid and normal urinary calcium, stone events occurred at 0.12 per patient a year on allopurinol 100 mg three times a day and 0.26 on placebo, and time to recurrence was longer on allopurinol. Against their own history, stones fell 81.2% on allopurinol and 63.4% on placebo [8].
Population: 60 people with a history of calcium oxalate stones [8].
Sources: [8]
Caveats: One small trial from 1986. Stones also fell 63.4% in the placebo group, which the authors attribute to the bias of comparing people against their own history [8].

DulaglutideLimited

Kidney outcomes in type 2 diabetes

One large trial found a 15% lower rate of a combined kidney outcome on dulaglutide, mostly from less new heavy protein in the urine.

Compared with placebo [7]

The numbers and sources

Effect: The kidney outcome, new macroalbuminuria, a sustained 30% or greater fall in eGFR, or chronic kidney replacement, occurred in 17.1% on dulaglutide and 19.6% on placebo (HR 0.85, 95% CI 0.77 to 0.93). New macroalbuminuria fell (HR 0.77, 95% CI 0.68 to 0.87), while the eGFR decline (HR 0.89, 95% CI 0.78 to 1.01) and kidney replacement therapy (HR 0.75, 95% CI 0.39 to 1.44) did not differ significantly [7].
Population: 9,901 adults with type 2 diabetes in REWIND, mean eGFR 76.9, followed a median 5.4 years [7].
Sources: [7]
Caveats: An exploratory analysis of a cardiovascular trial, funded by the manufacturer [7].
Why limited: This rests on one trial, of 9,901 people. Strength counts independent studies that agree, so one trial is limited at any size.

SemaglutideLimited

Kidney disease in type 2 diabetes

One trial found a 24% lower risk of major kidney events, and fewer deaths, in adults with type 2 diabetes and chronic kidney disease.

The numbers and sources

Effect: Major kidney disease events (kidney failure, a fall in eGFR of 50% or more, or death from kidney or cardiovascular causes) occurred in 331 people on semaglutide and 410 on placebo (HR 0.76, 95% CI 0.66 to 0.88). The kidney-specific events alone gave HR 0.79 (95% CI 0.66 to 0.94). eGFR declined 1.16 mL/min/1.73 m2 a year more slowly, cardiovascular death was lower (HR 0.71, 95% CI 0.56 to 0.89) and death from any cause was lower (HR 0.80, 95% CI 0.67 to 0.95) [6].
Population: 3,533 adults with type 2 diabetes and chronic kidney disease with raised urine albumin, 1.0 mg weekly, median follow-up 3.4 years [6].
Sources: [6]
Caveats: One trial, stopped early after a prespecified interim analysis. Funded by Novo Nordisk. It enrolled people with type 2 diabetes, so it does not describe kidney disease without diabetes [6].
Why limited: This rests on one trial, of 3,533 people. Strength counts independent studies that agree, so one trial is limited at any size.

Loop diureticsModerate

Preventing or treating acute kidney injury

Mixed results: furosemide did not change deaths or dialysis in kidney injury, while a Cochrane review found less new injury when diuretics were given beforehand.

Compared with placebo or usual care [11]; placebo, no treatment or intravenous fluids [12]

The numbers and sources

Effect: In adults with or at risk of acute kidney failure, furosemide did not change in-hospital mortality (RR 1.11, 95% CI 0.92 to 1.33), need for dialysis (RR 0.99, 95% CI 0.80 to 1.22) or persistent low urine output [11]. For treating established injury, diuretics made little or no difference to dialysis (RR 0.93) or death (RR 1.08) and raised hypotension and arrhythmias. For prevention, diuretics lowered new kidney injury (RR 0.75, 95% CI 0.61 to 0.92, low certainty), dialysis (RR 0.63) and death (RR 0.73) [12].
Population: 849 patients in 9 furosemide trials [11]; 9,871 people in 64 studies, 8,078 in prevention studies [12].
Sources: [11], [12]
Caveats: [12] pooled diuretics as a group, not loop diuretics alone, and the prevention finding had high heterogeneity (I² 77%).

Thiazide diureticsModerate

Kidney stone prevention

Mixed results: a pooled analysis of 10 trials found 37% fewer stone recurrences on thiazides, and the largest trial found no difference from placebo.

The numbers and sources

Effect: A meta-analysis of 10 randomized trials found fewer stone recurrences on thiazides than placebo (RR 0.63, 95% CI 0.49 to 0.83), with substantial heterogeneity (I² 65%) [12]. In the largest trial, symptomatic or radiologic recurrence occurred in 59% on placebo and in 59%, 56% and 49% on hydrochlorothiazide 12.5, 25 and 50 mg, with no relation between dose and recurrence (P = 0.66) [13].
Population: 650 people on thiazides and 672 on placebo in 10 trials [12]; 416 people with recurrent calcium-containing kidney stones followed a median 2.9 years [13].
Sources: [12], [13]
Caveats: The pooled trials are mostly older and smaller than [13]. Not an FDA-approved use [14].

AllopurinolModerate

Slowing chronic kidney disease

Not shown to slow loss of kidney function in two placebo-controlled trials, in chronic kidney disease and in type 1 diabetes.

The numbers and sources

Effect: In adults with stage 3 or 4 chronic kidney disease, eGFR fell 3.33 mL/min/1.73 m² a year on allopurinol and 3.23 on placebo (difference -0.10, 95% CI -1.18 to 0.97) [9]. In people with type 1 diabetes and early kidney disease, serum urate fell from 6.1 to 3.9 mg/dL on allopurinol and stayed at 6.1 on placebo. Measured GFR after 3 years and a washout did not differ (difference 0.001, 95% CI -1.9 to 1.9), and urinary albumin excretion was 40% higher on allopurinol (95% CI 0 to 80) [10].
Population: 363 adults with chronic kidney disease, no gout and a mean eGFR of 31.7, followed 104 weeks [9]; 530 people with type 1 diabetes and a GFR of 40 to 99.9 [10].
Sources: [9], [10]
Caveats: The first trial stopped recruiting early, at 369 of a planned 620 people [9].

Alpha-blockersModerate

Small ureteral stones in large placebo-controlled trials

Not shown to help small ureteral stones pass in two large trials, where tamsulosin and placebo gave the same rates, 81% against 80% and 50% against 47%.

Compared with placebo and nifedipine [11]; placebo [12]

The numbers and sources

Effect: In a UK trial, 81% on tamsulosin 400 µg, 80% on nifedipine and 80% on placebo needed no further intervention by 4 weeks (adjusted risk difference for tamsulosin 1.3%, 95% CI -5.7 to 8.3) [11]. In a US emergency department trial with a mean stone size of 3.8 mm, 50% passed the stone by day 28 on tamsulosin 0.4 mg and 47% on placebo (RR 1.05, 95.8% CI 0.87 to 1.27), and no secondary outcome differed [12].
Population: 1,136 adults aged 18 to 65 with a single ureteral stone of 10 mm or less at 24 UK hospitals [11]; 497 adults with stones under 9 mm at 6 US emergency departments [12].
Sources: [11], [12]
Caveats: Most stones in both trials were small, the group where the meta-analyses also found little effect [9][10]. The US trial excluded people lost to follow-up before stone passage [12].

Supplements

CordycepsModerate

Kidney function

Shown to lower serum creatinine and urine protein when added to treatment in chronic kidney disease, in low-quality trials.

The numbers and sources

Effect: In a Cochrane review of 22 studies (1,746 participants), Cordyceps preparations added to conventional treatment lowered serum creatinine by 60.76 µmol/L (14 studies), raised creatinine clearance by 9.22 mL/min (6 studies) and cut 24-hour proteinuria by 0.15 g (4 studies) in people not on dialysis [6]. A 2025 meta-analysis of 15 studies (1,310 patients) with kidney dysfunction, including acute kidney injury, found Cordyceps sinensis as an add-on lowered blood creatinine, shortened the period of low urine output and raised urine osmolality [7].
Population: People with chronic kidney disease [6]; people with kidney dysfunction, including acute kidney injury [7].
Sources: [6], [7]
Caveats: Both reviews rest on low-quality trials. Risk of bias was high in 4 studies and unclear in 18, and the Cochrane authors could not reach definitive conclusions [6]. The 2025 review reported overall efficacy as diagnostic accuracy statistics, gives no size for the creatinine change in its abstract, and found results differed between northern and southern Chinese patients [7].

Lab markers

Cystatin CStrong

Death from any cause

Linked to more deaths at higher levels, and a cystatin C-based kidney estimate at least 30% below the creatinine-based one went with 69% more deaths.

The numbers and sources

Effect: In elderly US adults, hazard ratios for death rose across fifths of cystatin C, from 1.08 (95% CI 0.86 to 1.35) in the second fifth to 2.58 (2.03 to 3.27) in the top part of the highest fifth, while creatinine showed a J-shaped association [11]. In a meta-analysis of 16 cohorts, being reclassified to a lower kidney function category by cystatin C than by creatinine went with a higher risk of death, and to a higher category with a lower risk, with a net reclassification improvement for death of 0.23 (95% CI 0.18 to 0.28) [12]. In 440,526 UK adults, the cystatin C-based estimate of kidney function was the one most strongly associated with cardiovascular disease and death [13]. Across 23 outpatient cohorts, people whose cystatin C-based estimate was at least 30% lower than their creatinine-based one had 28.4 deaths per 1,000 person-years against 16.8 in those whose two estimates were within 30% (HR 1.69, 95% CI 1.57 to 1.82) [14].
Population: 4,637 participants of the Cardiovascular Health Study [11]. 90,750 participants in 11 general-population studies and 2,960 in 5 cohorts with chronic kidney disease, 13,202 deaths [12]. 440,526 UK Biobank participants [13]. 821,327 people in 23 outpatient cohorts, mean follow-up 11 years [14].
Sources: [11], [12], [13], [14]
Caveats: Observational. Cystatin C rises with inflammation, smoking and other conditions apart from kidney function [2][15], so a high level may mark illness already present.

Cystatin CStrong

Heart attack, stroke and heart failure in cohort studies

Linked to more cardiovascular disease at higher levels, about 82% more for each doubling of cystatin C across 16 pooled cohorts.

The numbers and sources

Effect: Across 16 prospective cohorts, the relative risk of cardiovascular disease was 1.82 per doubling of cystatin C (95% CI 1.56 to 2.13) after adjustment for age, sex and traditional risk factors [16]. In elderly US adults, the highest fifth of cystatin C (1.29 mg/L or above) against the two lowest (0.99 mg/L or below) had hazard ratios of 2.27 (95% CI 1.73 to 2.97) for cardiovascular death, 1.48 (1.08 to 2.02) for heart attack and 1.47 (1.09 to 1.96) for stroke, while the highest fifth of creatinine was not associated with any of the three [11]. Among elderly adults without chronic kidney disease, each 0.18 mg/L higher went with hazard ratios of 1.28 (1.17 to 1.40) for heart failure, 1.22 (1.08 to 1.38) for stroke and 1.20 (1.06 to 1.36) for heart attack [10]. In 23 outpatient cohorts, a cystatin C-based kidney estimate at least 30% below the creatinine-based one went with hazard ratios of 1.35 (1.27 to 1.44) for atherosclerotic cardiovascular disease and 1.54 (1.40 to 1.68) for heart failure [14].
Population: 76,481 participants in 16 cohorts, 37,126 with cystatin C measured [16]. 4,637 elderly adults followed from 1992 or 1993 to 2001 [11]. 4,663 elderly adults, 78% without chronic kidney disease, median follow-up 9.3 years [10]. 821,327 outpatients [14].
Sources: [16], [11], [10], [14]
Caveats: Observational. The genetic analysis in the next block was run to test whether this link is causal and did not support it [16].

Estimated GFR (eGFR)Strong

Death from any cause and from cardiovascular disease

Linked to more deaths at lower eGFR: against 95, risk was 18% higher at 60, 57% higher at 45 and about 3 times higher at 15.

The numbers and sources

Effect: In a collaborative meta-analysis of general population cohorts, risk of death was unrelated to eGFR between 75 and 105 mL/min/1.73 m2 and rose at lower values. Against an eGFR of 95, adjusted hazard ratios for death from any cause were 1.18 (95% CI 1.05 to 1.32) at 60, 1.57 (1.39 to 1.78) at 45 and 3.14 (2.39 to 4.13) at 15, with similar findings for cardiovascular death [6]. In a later individual-participant analysis of 114 cohorts, lower eGFR was significantly associated with higher all-cause and cardiovascular mortality, including in the mildest categories of chronic kidney disease [7].
Population: 105,872 participants in 14 studies with urine albumin-to-creatinine measurements and 1,128,310 in 7 studies with dipstick measurements [6]. 27,503,140 individuals in 114 cohorts, mean age 54, mean follow-up 4.8 years [7].
Sources: [6], [7]
Caveats: Observational. Urine albumin predicted death independently of eGFR, so eGFR alone gives part of the picture [6]. KDIGO notes that creatinine-based eGFR has a J-shaped association with most outcomes, with risk also rising above 105 mL/min/1.73 m2, and that very low creatinine often reflects frailty or low muscle mass [3].

Estimated GFR (eGFR)Strong

Kidney failure

Linked to far more kidney failure at lower eGFR: against 95, the hazard was 4 times higher at 60, 29 times at 45 and 454 times at 15.

The numbers and sources

Effect: In general population cohorts, risk of end-stage renal disease was unrelated to eGFR between 75 and 105 mL/min/1.73 m2 and rose exponentially below that. Against an eGFR of 95, hazard ratios were 4 at an eGFR averaging 60, 29 at 45 and 454 at 15, after adjustment for albuminuria and cardiovascular risk factors. Similar associations were found for acute kidney injury and progressive chronic kidney disease [8]. A later analysis of 114 cohorts found lower eGFR associated with higher risk of kidney failure requiring replacement therapy and of acute kidney injury [7].
Population: 845,125 participants in 9 general population cohorts and 173,892 patients in 8 cohorts at high risk of chronic kidney disease [8]. 27,503,140 individuals in 114 cohorts [7].
Sources: [8], [7]
Caveats: Observational. These are relative hazards, and the abstract gives no absolute rates. Urine albumin predicted kidney failure independently of eGFR [8].

HemoglobinStrong

Stroke, clots and death in kidney disease trials that raised hemoglobin

Shown in kidney disease trials: aiming for a higher hemoglobin with erythropoietin-type drugs raised stroke, blood pressure and access clotting, and did not lower deaths.

The numbers and sources

Effect: In a meta-analysis of 9 trials, a higher hemoglobin target carried a higher risk of death from any cause (risk ratio 1.17, 95% CI 1.01 to 1.35) and of clotting in the dialysis access (1.34, 1.16 to 1.54) than a lower target [12]. A later meta-analysis of 27 trials found that a higher target raised stroke (relative risk 1.51, 95% CI 1.03 to 2.21), hypertension (1.67, 1.31 to 2.12) and access clotting (1.33, 1.16 to 1.53). Differences in death (1.09, 0.99 to 1.20) and serious cardiovascular events (1.15, 0.98 to 1.33) did not reach significance [13].
Population: 5,143 patients with anemia from chronic kidney disease in 9 randomized trials [12]. 10,452 patients in 27 trials [13].
Sources: [12], [13]
Caveats: These trials raised hemoglobin with erythropoiesis-stimulating drugs in people with kidney disease, so they do not show what a higher hemoglobin reached another way does in other people. The second analysis could not separate the effect of the drug dose from the effect of the hemoglobin reached [13].

Hemoglobin A1c (HbA1c)Strong

Eye, kidney and nerve complications of diabetes

Shown in trials: intensive glucose control that lowered HbA1c about 0.9 points cut kidney events 20% and eye events 13% in type 2 diabetes.

The numbers and sources

Effect: In an individual-participant meta-analysis of 4 trials in type 2 diabetes, more intensive control left HbA1c 0.90 percentage points lower (95% CI 0.58 to 1.22) and reduced kidney events (HR 0.80, 95% CI 0.72 to 0.88) and eye events (HR 0.87, 95% CI 0.76 to 1.00), with no reduction in nerve events (HR 0.98, 95% CI 0.87 to 1.09) [11]. In type 1 diabetes, intensive therapy reduced the development of retinopathy by 76% (95% CI 62 to 85) and clinical neuropathy by 60% (95% CI 38 to 74) [12]. In an observational analysis of people with type 2 diabetes, each 1% lower updated mean HbA1c went with 37% fewer microvascular complications (95% CI 33 to 41), with no threshold [13]. In pooled data from nine studies, diabetes-specific retinopathy was rare below 6.0% and its threshold fell at 6.3 to 6.7% [14].
Population: 27,049 adults with type 2 diabetes in 4 trials, median follow-up 5.0 years [11]. 1,441 people with type 1 diabetes followed a mean 6.5 years [12]. 3,642 people with type 2 diabetes [13]. 28,010 people with HbA1c and retinal photographs [14].
Sources: [11], [12], [13], [14]
Caveats: The trials tested treatment strategies, not HbA1c itself. Intensive therapy raised severe hypoglycemia two to threefold in the type 1 diabetes trial [12].

Urine albumin to creatinine ratioStrong

Death from any cause and cardiovascular death

Linked to more deaths at higher ratios with no threshold, 63% more at about 30 mg/g than at about 5 mg/g across 105,872 people.

The numbers and sources

Effect: In a meta-analysis of general population cohorts, the ratio was related to death on a continuous scale without a threshold. Against a ratio of 0.6 mg/mmol (about 5 mg/g), the adjusted hazard ratio for death from any cause was 1.20 (95% CI 1.15 to 1.26) at 1.1 mg/mmol (10 mg/g), 1.63 (1.50 to 1.77) at 3.4 mg/mmol (about 30 mg/g) and 2.22 (1.97 to 2.51) at 33.9 mg/mmol (about 300 mg/g). Findings were similar for cardiovascular death, and the ratio and estimated GFR each added risk without interaction [5]. In a later meta-analysis of 114 cohorts, higher ratios were associated with higher rates of each of 10 outcomes studied: kidney failure, death from any cause, cardiovascular death, acute kidney injury, hospitalization, coronary heart disease, stroke, heart failure, atrial fibrillation and peripheral artery disease [8].
Population: 105,872 participants in 14 general population cohorts with ratio measurements [5]. 9,067,753 people with albuminuria data in 114 cohorts, with a median ratio of 11 mg/g in the main population [8].
Sources: [5], [8]
Caveats: Observational, with the ratio measured once at baseline. The first meta-analysis printed its ratios in mg/mmol, and the mg/g figures other than 10 are converted here with the factor on this page [5].

Cystatin CModerate

Kidney failure and new chronic kidney disease

Linked to later kidney disease: elderly adults with normal creatinine-based kidney function and cystatin C of 1.0 mg/L or above had 4 times the risk.

The numbers and sources

Effect: Among elderly adults without chronic kidney disease, those with cystatin C of 1.0 mg/L or above had a 4-fold risk of progressing to chronic kidney disease after 4 years, compared with those below 1.0 mg/L [10]. In a meta-analysis of 16 cohorts, reclassification to a lower kidney function category by cystatin C went with a higher risk of end-stage renal disease, with a net reclassification improvement of 0.10 (95% CI 0.00 to 0.21) [12]. In 23 outpatient cohorts, a cystatin C-based estimate at least 30% below the creatinine-based one went with a hazard ratio of 1.29 (95% CI 1.13 to 1.47) for kidney failure with replacement therapy [14].
Population: 4,663 elderly adults in a US community cohort [10]. 1,654 cases of end-stage renal disease in 7 cohorts [12]. 821,327 outpatients [14].
Sources: [10], [12], [14]
Caveats: Observational. Cystatin C is itself a measure of kidney filtration, so a higher level at the start may reflect kidney function already lower than creatinine showed.

Estimated GFR (eGFR)Moderate

Heart disease, stroke, heart failure and hospital admission

Linked to more coronary heart disease, stroke, heart failure, atrial fibrillation and hospital admissions at lower eGFR in an analysis of 114 cohorts.

The numbers and sources

Effect: In an individual-participant meta-analysis, lower eGFR was significantly associated with higher risk of each of 10 outcomes studied, among them coronary heart disease, stroke, heart failure, atrial fibrillation, peripheral artery disease and any hospitalization. Among people with a urine albumin-to-creatinine ratio below 10 mg/g, an eGFR of 45 to 59 against 90 to 104 mL/min/1.73 m2 went with more hospitalizations (adjusted HR 1.3, 95% CI 1.2 to 1.3), 161 against 79 events per 1,000 person-years [7].
Population: 27,503,140 individuals from 114 global cohorts with creatinine-based eGFR, and 720,736 from 20 cohorts with eGFR based on creatinine and cystatin C, from 1980 to 2021 [7].
Sources: [7]
Caveats: Observational and retrospective. The analysis used the 2021 CKD-EPI equations. Confounding by age and other illness may remain after adjustment [7].

Estimated GFR (eGFR)Moderate

Kidney outcomes in trials of treatments that slowed eGFR decline

Shown in trials: across 47 trials of 12 interventions, treatments that slowed the yearly fall in GFR also reduced kidney failure and doubling of creatinine.

The numbers and sources

Effect: In a meta-analysis of 47 randomized trials, a treatment's effect on the 3-year slope of GFR predicted its effect on the clinical endpoint of doubling of serum creatinine, GFR below 15 mL/min/1.73 m2 or end-stage kidney disease (median R squared 0.97, 95% Bayesian credible interval 0.78 to 1.00). A treatment effect of 0.75 mL/min/1.73 m2 per year or greater on slope predicted a clinical benefit with at least 96% probability, given a large enough trial [9].
Population: 60,620 participants in 47 randomized trials testing 12 interventions, in people with chronic kidney disease [9].
Sources: [9]
Caveats: The trials enrolled people with kidney disease and tested drugs and other treatments, so the finding does not describe people with eGFR in the reference range. It concerns the rate of change over years, not one result [9].

Uric acid (serum urate)Moderate

Kidney stones

Linked to more kidney stones in men in one large Korean cohort, 72% more at 10 mg/dL or above, with no such pattern in women.

The numbers and sources

Effect: In 239,331 Korean adults having health checkups, men with higher uric acid developed more kidney stones in a dose-response pattern. Against below 6.0 mg/dL, adjusted hazard ratios were 1.06 (95% CI 1.02 to 1.11) at 6.0 to 6.9 mg/dL, 1.11 (1.05 to 1.16) at 7.0 to 7.9, 1.21 (1.13 to 1.29) at 8.0 to 8.9, 1.31 (1.17 to 1.46) at 9.0 to 9.9 and 1.72 (1.44 to 2.06) at 10.0 or above. No dose-response association was seen in women [13]. An umbrella review found that the one trial outcome with robust evidence for urate-lowering treatment was fewer recurrences of kidney stones [12].
Population: 239,331 adults with 18,777 new cases of kidney stones found on ultrasound [13]. 31 meta-analyses of randomized trials within the umbrella review [12].
Sources: [13], [12]
Caveats: The cohort is observational, had no dietary data and did not use CT to confirm stones [13].

Urine albumin to creatinine ratioModerate

Kidney failure

Linked to kidney failure, with a 30% fall in the ratio over 2 years tied to 17% lower risk of end-stage kidney disease across 28 cohorts.

The numbers and sources

Effect: In an individual-level meta-analysis, a 30% decrease in the ratio over 2 years was followed by a lower risk of end-stage kidney disease (adjusted HR 0.83, 95% CI 0.74 to 0.94, and 0.78 after correction for measurement variability). The association was stronger at higher starting ratios. In people starting at 300 mg/g or higher, a 30% fall was estimated to lower the 10-year risk of end-stage kidney disease by more than 1 percentage point [10]. A kidney guideline states that in large population studies a doubling of the ratio within 2 years is associated with a 50% to 100% higher risk of progression to kidney failure [4].
Population: 693,816 people in 28 cohorts, 80% with diabetes, with 7,461 end-stage kidney disease events [10].
Sources: [10], [4]
Caveats: Observational. A fall in the ratio in these cohorts had many causes, and the analysis does not show that lowering the ratio by any particular means changes the outcome [10].

Urine albumin to creatinine ratioModerate

Kidney outcomes in trials of treatments that lowered albuminuria

Shown across 41 trial comparisons that treatments lowering albuminuria by 30% went with 27% fewer kidney endpoints, less certain when starting albuminuria was low.

The numbers and sources

Effect: A meta-analysis related each treatment's effect on albuminuria at 6 months to its effect on a composite of end-stage kidney disease, estimated GFR below 15 mL/min per 1.73 m² or doubling of serum creatinine. Each 30% decrease in albuminuria relative to control was associated with an average 27% lower hazard of the composite (95% credible interval 5% to 45%). The association was stronger in patients with starting albuminuria above 30 mg/g [11].
Population: 29,979 participants in 41 treatment comparisons from randomized trials, 71% with diabetes, followed for a median of 3.4 years [11].
Sources: [11]
Caveats: A comparison across trials of different drugs, with a wide credible interval. The authors describe the association as less certain for patients with low albuminuria at baseline [11].

Blood urea nitrogen (BUN)Limited

Kidney failure in people with chronic kidney disease

One study of 459 people with stage 3 to 5 kidney disease found more kidney failure or death in the top quarter of BUN, independent of eGFR.

The numbers and sources

Effect: In 459 Japanese patients with chronic kidney disease stages 3 to 5 followed for a median of 25.8 months, hazard ratios for end-stage renal disease or death in the second, third and fourth quartiles of BUN against the first were 1.36 (95% CI 0.72 to 2.58), 1.87 (0.95 to 3.66) and 2.66 (1.23 to 5.76), after adjustment that included eGFR. Higher BUN quartiles also carried more risk of end-stage renal disease alone [9].
Population: 459 patients with chronic kidney disease stages 3 to 5, of whom 210 reached the endpoint [9].
Sources: [9]
Caveats: Observational, one cohort in one country. Only the top quartile differed significantly from the bottom [9].

FructosamineLimited

Eye and kidney complications

One US cohort linked fructosamine above the 95th percentile to 50% more new chronic kidney disease, and higher levels to more retinopathy.

The numbers and sources

Effect: Fructosamine and glycated albumin were strongly associated with retinopathy (P below 0.0001 for trend). The adjusted hazard ratio for chronic kidney disease was 1.50 (95% CI 1.22 to 1.85) for fructosamine above the 95th percentile and 1.48 (1.20 to 1.83) for glycated albumin, compared with people without diabetes below the 75th percentile. Prediction of chronic kidney disease was nearly as strong as with HbA1c, with C statistics of 0.717, 0.717 and 0.726 [5].
Population: 11,348 adults without diabetes and 958 with diagnosed diabetes, followed for two decades [5].
Sources: [5]
Caveats: Observational, from one cohort. A laboratory guideline states that few published studies have convincingly shown a relationship between glycated protein levels and the chronic complications of diabetes [2].

Parathyroid hormone (PTH)Limited

Kidney function

One study found PTH differed across tenths of kidney function in 1,814 patients, and 12% of those with an eGFR above 80 already had high PTH.

The numbers and sources

Effect: In outpatients tested across 153 centers, mean and median PTH differed significantly across deciles of estimated glomerular filtration rate (P below 0.001). High PTH, defined as above 65, was present in 12% of patients with an eGFR above 80 mL/min, while calcium and phosphorus stayed normal until eGFR fell below 40 [10]. Kidney guidelines set separate PTH targets for people on dialysis: the National Kidney Foundation's KDOQI guidelines used 150 to 300 pg/mL for stage 5 chronic kidney disease [11], and the KDIGO guideline uses two to nine times the upper limit of the assay [9]. The 2017 KDIGO update bases treatment on trends in results and not on a single abnormal value [12].
Population: 1,814 patients with a mean age of 71.1, 48% with diabetes [10].
Sources: [10], [11], [9], [12]
Caveats: Cross-sectional, in older patients, and the abstract misprints the unit of its PTH cut point. The dialysis targets are treatment targets for kidney failure and are not reference ranges. The KDIGO target is a multiple of each assay's upper limit, a different quantity from a result in pg/mL, so it has no band on this page.

Serum creatinineLimitedStudied in men

Stroke and death at higher levels

Limited evidence: one British cohort of 7,690 middle-aged men linked creatinine above 1.31 mg/dL to 60% more strokes over about 15 years.

The numbers and sources

Effect: Median creatinine was 98 µmol/L (1.11 mg/dL). Above 116 µmol/L (1.31 mg/dL), the top tenth, the relative risk of stroke was 1.6 (95% CI 1.1 to 2.1) against all other men after adjustment for cardiovascular risk factors. For major ischemic heart disease, the relative risk at 130 µmol/L (1.47 mg/dL) or above was 1.2 (0.8 to 1.7) after adjustment. Death from any cause and from cardiovascular disease was significantly raised only above the 97.5th percentile, and there was no association with death from cancer [6].
Population: 7,690 men aged 40 to 59 from 24 British towns, followed for an average of 14.75 years, with 287 strokes, 967 major ischemic heart disease events and 1,259 deaths [6].
Sources: [6]
Caveats: One observational cohort of middle-aged men in one country [6]. Studies that convert creatinine to an estimated filtration rate are covered on the eGFR page.

Serum creatinineLimited

Death in hospital after a rise during the stay

Limited evidence: in one hospital cohort a rise in creatinine of 0.5 mg/dL or more during the stay went with 6.5 times the odds of death.

The numbers and sources

Effect: Among adults with two or more creatinine results during a hospital stay, a rise of 0.5 mg/dL or more occurred in 1,237 (13%) and a rise of 2.0 mg/dL or more in 105 (1%). A rise of 0.5 mg/dL or more was associated with 6.5 times the odds of death (95% CI 5.0 to 8.5), 3.5 more days in hospital and nearly 7,500 dollars in added cost, after adjustment for age, sex, diagnosis, severity of illness and chronic kidney disease [7].
Population: 9,210 adults with two or more creatinine measurements, among 19,982 admitted to one urban academic medical center [7].
Sources: [7]
Caveats: Observational, at one center, in people ill enough to be admitted. It concerns a change during a hospital stay, not a single outpatient result [7].

Total iron binding capacity (TIBC)Limited

Death in people on hemodialysis

Limited evidence: one cohort of 807 hemodialysis patients linked a lower TIBC, and a fall in TIBC over 6 months, to more deaths.

The numbers and sources

Effect: Mortality rose step by step across lower TIBC groups. The adjusted hazard ratio for death was 1.75 (95% CI 1.00 to 3.05) for a TIBC below 150 against 200 to 250, and a fall of more than 20 over 6 months had a hazard ratio of 1.57 (1.04 to 2.36) against a stable result. Patients with a TIBC of 250 or above had a higher body mass index, more arm muscle and fat by skinfold, higher serum iron, and lower ferritin and inflammatory markers [7].
Population: 807 people on maintenance hemodialysis in a prospective 5-year cohort [7].
Sources: [7]
Caveats: One observational cohort in people on dialysis, in whom the authors treat TIBC as a marker of protein and energy wasting, so it does not describe people without kidney failure. The abstract prints the TIBC values in mg/dL, and the figures above are given as printed. The lower limit of the hazard ratio for a low TIBC is 1.00 [7].

Uric acid (serum urate)Moderate

Chronic kidney disease, in cohorts and in trials that lowered urate

Mixed results: cohorts link higher uric acid to new kidney disease, while two allopurinol trials found no slowing of kidney function decline.

The numbers and sources

Effect: In a meta-analysis of 13 cohort studies, higher serum uric acid went with more new chronic kidney disease (summary odds ratio 1.15, 95% CI 1.05 to 1.25), and hyperuricemia with an odds ratio of 2.35 (1.59 to 3.46) [18]. In a randomized trial in adults with stage 3 or 4 chronic kidney disease and a mean serum urate of 8.2 mg/dL, eGFR fell by 3.33 mL/min/1.73 m2 a year on allopurinol and 3.23 on placebo (difference -0.10, 95% CI -1.18 to 0.97) [19]. In a randomized trial in people with type 1 diabetes and early kidney disease, allopurinol lowered mean serum urate from 6.1 to 3.9 mg/dL, and measured GFR after 3 years and a 2-month washout did not differ from placebo (difference 0.001 mL/min/1.73 m2, 95% CI -1.9 to 1.9) [20]. KDIGO's 2024 guideline suggests against using urate-lowering drugs to delay kidney disease progression in people with chronic kidney disease whose hyperuricemia causes no symptoms [3].
Population: 190,718 participants in 13 studies [18]. 363 patients analyzed, mean eGFR 31.7 mL/min/1.73 m2 [19]. 530 participants with type 1 diabetes, mean age 51.1 [20].
Sources: [18], [19], [20], [3]
Caveats: The first trial stopped early for slow recruitment after enrolling 369 of 620 intended patients [19]. The cohort finding is observational, and reverse causation, with early kidney decline raising uric acid, cannot be ruled out.

HematocritLimited

Death and heart attack in a dialysis trial that raised hematocrit to 42%

One trial found raising hematocrit to 42% with epoetin did not cut deaths or heart attacks in hemodialysis patients with heart disease, and the trial was halted.

The numbers and sources

Effect: Patients were assigned to epoetin doses aimed at a hematocrit of 42% or of 30%. After 29 months there were 183 deaths and 19 first nonfatal heart attacks in the 42% group and 150 deaths and 14 nonfatal heart attacks in the 30% group, a risk ratio of 1.3 (95% CI 0.9 to 1.9). The difference did not reach the preset stopping boundary, and the study was halted. Within each group, death rates fell as the hematocrit reached rose [11].
Population: 1,233 people on hemodialysis with heart failure or ischemic heart disease, treated for a median of 14 months [11].
Sources: [11]
Caveats: One trial in people on dialysis with heart disease, in whom hematocrit was raised with a drug. The higher target group also had a decline in the adequacy of dialysis and more intravenous iron, so the trial cannot separate hematocrit from the treatment used to raise it [11].
Why limited: This rests on one trial, of 1,233 people. Strength counts independent studies that agree, so one trial is limited at any size.

Parathyroid hormone (PTH)Limited

Death and cardiovascular events in a trial of cinacalcet in dialysis patients

One trial found cinacalcet, a drug for raised PTH, did not significantly reduce death or cardiovascular events in dialysis patients: 48.2% against 49.2% on placebo.

The numbers and sources

Effect: In patients on hemodialysis with moderate to severe secondary hyperparathyroidism, the composite of death, heart attack, hospitalization for unstable angina, heart failure or a peripheral vascular event occurred in 938 of 1,948 (48.2%) on cinacalcet and 952 of 1,935 (49.2%) on placebo, a relative hazard of 0.93 (95% CI 0.85 to 1.02, P = 0.11). Low blood calcium and gastrointestinal adverse events were significantly more frequent on cinacalcet [14].
Population: 3,883 patients with a median intact PTH of 693 pg/mL, followed for up to 64 months [14].
Sources: [14]
Caveats: A marker that tracks an outcome is not always one whose correction changes it. This is the unadjusted intention-to-treat result, and the trial was funded by the drug's maker. It studied people with kidney failure and very high PTH, so it says nothing about results near the reference range [14].
Why limited: This rests on one trial, of 3,883 people. Strength counts independent studies that agree, so one trial is limited at any size.