Kidney Disease: Which Blood & Urine Tests Do You Need?

The kidneys filter about 180 liters of blood a day through roughly two million glomeruli. Chronic kidney disease (CKD) is a loss of that filtering capacity, or damage to the filters, that has lasted more than three months. The definition in the KDIGO guideline is precise: an estimated glomerular filtration rate (eGFR) below 60 mL/min/1.73 m², or a marker of kidney damage — most often albumin leaking into the urine at 30 mg per gram of creatinine or more — on two tests at least three months apart.

Nothing hurts while this happens. The kidneys have so much reserve that fatigue, swelling, foamy urine, nocturia, itching, nausea and muscle cramps usually appear only when the eGFR has fallen below 30 — by which point most of the filtering capacity is gone. About one adult in seven has CKD and roughly nine in ten of them do not know it. The two tests exist because the disease cannot be felt, and because the treatments that slow it — blood-pressure and glucose control, ACE inhibitors or ARBs, SGLT2 inhibitors, and more recently finerenone and GLP-1 agonists — work best early.

Creatinine and eGFR. Creatinine is a waste product of muscle that the kidneys clear at a steady rate; the lab converts it into an eGFR using the 2021 CKD-EPI equation (age and sex, no race term). An eGFR of 90 or more is normal (G1), 60–89 mildly reduced (G2 — normal for many older adults and not CKD on its own without a damage marker), 45–59 is G3a, 30–44 G3b, 15–29 G4 and below 15 is kidney failure (G5). Creatinine depends on muscle mass, so a very muscular person, a creatine user or someone who ate a large meat meal reads a little high, and a frail or amputee patient reads falsely well.

Cystatin C. A small protein made by every cell at a constant rate and cleared only by the kidneys. It is not affected by muscle mass or diet, so a cystatin C eGFR (or the combined creatinine-cystatin equation) is the KDIGO-recommended confirmation when a creatinine eGFR of 45–59 has no other marker of damage, when muscle mass is unusual, or when the number will change a treatment decision. It is affected by thyroid disease, steroids, smoking and obesity.

Urine albumin-to-creatinine ratio (UACR). A spot urine sample, ideally first-morning, that reports albumin corrected for how dilute the urine is. Below 30 mg/g is normal (A1), 30–300 moderately increased (A2 — what used to be called microalbuminuria) and above 300 severely increased (A3). Albuminuria is the earliest sign of diabetic and hypertensive kidney disease, often years before eGFR moves, and it independently predicts heart attack, stroke and progression to failure. A dipstick protein is not a substitute; it misses the 30–300 range.

Urinalysis with microscopy. Blood, protein, white cells, casts and crystals point to the cause: dysmorphic red cells and red-cell casts mean glomerular disease and a prompt nephrology referral; white-cell casts mean infection or interstitial nephritis; granular casts and tubular cells mean tubular injury.

The rest of the renal or comprehensive metabolic panel. BUN rises with eGFR and with dehydration; potassium rises as the kidneys fail to excrete it and with ACE inhibitors and ARBs; bicarbonate falls as acid accumulates; calcium falls and phosphorus rises as the kidneys stop activating vitamin D and clearing phosphate, which drives parathyroid hormone up (CKD mineral and bone disorder, usually from stage 3b); albumin falls with heavy protein loss. A CBC adds the anemia of CKD, which begins as erythropoietin production falls from stage 3. Hemoglobin A1c and a lipid panel address the two conditions that cause and accompany most CKD.

• Diabetes — eGFR and UACR at diagnosis of type 2 (five years after diagnosis of type 1) and every year after; the ADA and KDIGO agree. Albuminuria is where diabetic kidney disease is caught and where SGLT2 inhibitors and finerenone change the course.
• High blood pressure — both tests yearly; hypertension is the second leading cause of CKD and CKD raises blood pressure in turn.
• Cardiovascular disease, heart failure, obesity, a family history of kidney disease or dialysis, age over 60 — both tests, repeated every one to three years depending on the result.
• Regular NSAID, lithium or proton-pump inhibitor use, a history of acute kidney injury, kidney stones, lupus or another autoimmune disease, HIV, hepatitis B or C, gout, polycystic kidney disease in the family — a baseline eGFR and UACR, then as advised.
• Anyone with foamy urine, new swelling of the ankles or around the eyes, blood in the urine, unexplained anemia or a raised creatinine on a routine panel — the full workup now, including a urinalysis with microscopy.

The USPSTF does not recommend screening adults without risk factors, and a single routine eGFR in a healthy younger adult is reassurance rather than a program. For everyone on the list above, the pair of tests once a year is the standard of care.

Preparation. Skip hard exercise, creatine supplements and a large cooked-meat meal for 24 hours before a creatinine; drink normally. Collect the urine sample first thing in the morning if you can, not during a period, a urinary infection or a fever, and not within 72 hours of strenuous exercise — all of which raise albumin for a short time. Fasting is only needed for the glucose on the metabolic panel.

KDIGO stages CKD on a grid of eGFR (G1–G5) against albuminuria (A1–A3), because the two predict different things and together predict outcome. G1–G2 with A1 is not CKD. G3a with A1 (eGFR 45–59, normal albumin) is mild CKD and common over 70; it is confirmed with cystatin C and managed with blood pressure, glucose and a medication review. Any A2 or A3 — albumin at 30 mg/g or more — is CKD at any eGFR and is treated, because albuminuria is both a marker and a driver of progression. G3b and below, or A3 at any eGFR, moves to the moderate- and high-risk cells where anemia, mineral and bone disorder, acidosis and potassium start to need monitoring every three to six months.

Chronicity matters: one low eGFR is not CKD. Dehydration, an NSAID, a contrast scan or an illness can drop the number for days to weeks (acute kidney injury), and the diagnosis needs a repeat after three months. A fall of more than 25% in eGFR, or more than 5 mL/min a year, is rapid progression and is referred regardless of stage. The KDIGO referral triggers are an eGFR below 30, a UACR above 300 mg/g, hematuria with proteinuria, persistent potassium abnormalities, refractory hypertension, recurrent stones and hereditary kidney disease.

Two common patterns deserve naming. A young, muscular person with an eGFR of 70–85 and a normal UACR almost always has a creatinine artifact; cystatin C settles it. A person with diabetes, an eGFR of 95 and a UACR of 80 has early diabetic kidney disease despite the "normal" eGFR and is exactly the patient the treatments were designed for.

Order the panel online, walk into any Quest or Labcorp location with your requisition — no appointment or doctor's visit needed — and results post to your account, most within one to two business days. The blood draw and the urine sample are collected at the same visit; bring a first-morning urine sample from home if the location allows it, or give one on site.

Take an abnormal result to your clinician: a confirmatory repeat at three months decides whether it is CKD, and the treatment — blood-pressure control to below 130/80, an ACE inhibitor or ARB when albumin is present, an SGLT2 inhibitor for most people with CKD and diabetes or albuminuria, statin therapy, glucose control, avoiding NSAIDs and adjusting other drug doses — is prescription territory. A nephrology referral follows the triggers above. Results that show an eGFR below 15, a potassium above 6 mmol/L, or symptoms of confusion, breathlessness, vomiting or very little urine need same-day care.