Chronic Kidney Disease: Frequently Asked Questions

eGFR stands for estimated Glomerular Filtration Rate. It indicates how well your kidneys are filtering waste from your blood in mL/min/1.73m². A score of 60 or higher is generally normal. If your score stays below 60 for 3 months or more, it confirms Chronic Kidney Disease (CKD).

CKD has 5 stages based on eGFR: Stage G1 (eGFR ≥90) normal; Stage G2 (eGFR 60-89) mild reduction; Stage G3a (eGFR 45-59) mild-to-moderate; Stage G3b (eGFR 30-44) moderate-to-severe; Stage G4 (eGFR 15-29) severe; and Stage G5 (eGFR <15) kidney failure.

UACR (Urine Albumin-to-Creatinine Ratio) measures protein leakage into the urine. It is an early marker of kidney damage. A value under 30 mg/g is normal, 30–300 mg/g is moderately increased, and over 300 mg/g is severely increased, representing high risk.

Creatinine is a raw waste product from muscles. eGFR is a standardized score calculated from creatinine, age, and sex to represent actual filtration rate. Raw creatinine can vary with muscle mass, while eGFR normalizes this variance.

UACR categories: A1 is normal (<30 mg/g); A2 is moderately increased microalbuminuria (30–300 mg/g); and A3 is severely increased macroalbuminuria (>300 mg/g), indicating significant glomerular barrier breakdown.

Early-stage CKD (Stages G1–G3a) is typically asymptomatic. Kidney damage is usually only detected through blood or urine testing during routine medical screening.

Advanced symptoms (Stages G4–G5) include fluid retention (swelling in ankles and hands), fatigue, shortness of breath, nausea, vomiting, metallic taste in the mouth, and intense skin itching.

On average, eGFR decline is 1 to 3 points per year. A loss of 5 points or more in one year is considered rapid progression, requiring prompt medical intervention to slow the decline.

Nephrology referral is recommended when eGFR falls below 30 mL/min/1.73m², when eGFR decline is rapid (≥5 points/year), or when urine protein leakage is high (UACR >300 mg/g).

High blood pressure scars and hardens the kidneys' micro-vessels. Diabetes causes high blood sugar that damages the delicate filtering units (nephrons). Together they are the primary causes of chronic kidney disease.

Patients should limit high-potassium foods (bananas, potatoes, tomatoes) and foods containing inorganic phosphorus additives (dark colas, processed meats, fast foods). Avoid excessive protein intake pre-dialysis.

For advanced CKD, the daily potassium limit is usually restricted to under 2,000 mg. Double-boiling and leaching potatoes and root vegetables can wash out 50% to 75% of their potassium content.

Normal potassium is 3.5 to 5.0 mEq/L. Hyperkalemia is mild at 5.1-5.5, moderate at 5.6-5.9 (requires intervention), and severe at ≥6.0 mEq/L, representing a medical emergency that requires an ECG.

Hyperkalemia is often asymptomatic. If symptoms occur, they include muscle weakness, fatigue, numbness, tingling, palpitations, and chest tightness.

Pre-dialysis patients at G3b–G5 should target 0.6–0.8 g/kg/day to minimize nitrogenous uremic toxins. On dialysis, protein requirements increase to 1.1–1.4 g/kg/day to prevent protein-energy wasting.

PRAL measures the net acid load produced by foods. Positive PRAL foods (meat, poultry, cheese) produce metabolic acid. Negative PRAL foods (fruits, vegetables) produce alkali buffers, helping prevent metabolic acidosis.

Plant organic phosphorus is phytate-bound and only 30-40% is absorbed. Chemical inorganic phosphorus additives (found in processed foods) are not protein-bound and are absorbed at a rate of 100%.

Inorganic additives cause rapid spikes in blood phosphorus levels, leading to arterial hardening, cardiovascular calcification, bone disease, and increased mortality risk.

Phosphate binders are medications taken with meals. They bind to dietary phosphorus in the stomach and intestines, forming insoluble complexes that are excreted in stool rather than absorbed.

No. Potassium chloride salt substitutes contain high amounts of potassium and can trigger severe, life-threatening hyperkalemia in patients with moderate to advanced kidney disease.

Metformin is safe when eGFR ≥45. Lower the dose to a max of 1,000 mg/day for eGFR 30–44. It is contraindicated at eGFR <30 due to the risk of Metformin-Associated Lactic Acidosis (MALA).

Yes. KDIGO 2024 guidelines recommend initiating SGLT2 inhibitors down to eGFR 20 to protect kidneys, reduce proteinuria, and lower cardiovascular risk, regardless of diabetic status.

Finerenone is a non-steroidal mineralocorticoid receptor antagonist (MRA) that reduces eGFR decline and cardiovascular events in diabetic CKD. Do not start if potassium is >5.0 mEq/L.

They protect kidneys long-term, although an initial 10-20% eGFR drop is normal. They must be monitored for hyperkalemia and held temporarily during acute illness or volume depletion.

The co-administration of an NSAID (like ibuprofen), an ACEi or ARB (like lisinopril), and a diuretic (like furosemide). This combination blocks kidney compensatory mechanisms, leading to acute kidney injury.

It is the temporary suspension of certain kidney medications (SGLT2 inhibitors, Metformin, ACEi/ARBs, and diuretics) during acute illnesses with dehydration (diarrhea, vomiting, fever) to prevent acute kidney injury.

Yes. A plant-dominant low-protein diet (PLADO) lowers phosphorus load and acid load, which helps preserve kidney function. However, serum potassium must be monitored regularly.

In advanced CKD (G3-G5), parathyroid hormone levels are managed within a target range of 2 to 9 times the upper limit of normal for the lab assay to prevent mineral bone disorder.

Declining kidney function leads to phosphorus buildup and impaired Vitamin D activation. This causes calcium levels to drop, prompting the parathyroid glands to pull calcium out of bones.

Kidneys produce erythropoietin (EPO), a hormone that stimulates red blood cell production. Damaged kidneys produce less EPO, causing anemia. Treatment includes iron supplements and EPO-stimulating agents.

Dialysis is started based on symptoms (such as severe uremic symptoms, fluid overload, persistent nausea, and vomiting) rather than a strict eGFR cutoff, as demonstrated by the IDEAL trial.

Haemodialysis uses an external machine with a dialyzer filter to clean blood, typically done in a center. Peritoneal dialysis uses the abdomen lining as a filter and is performed daily at home.

CKM is an active, non-dialysis treatment plan focusing on symptom relief, cardiovascular support, and maintaining quality of life for advanced kidney failure patients.

An AV (arteriovenous) fistula is a surgical connection between an artery and a vein in the arm. It is preferred for haemodialysis because it has the lowest risk of blood clots and infections.

Dialysis filters out essential amino acids, requiring patients to increase their protein intake to 1.1–1.4 g/kg/day to prevent protein-energy wasting and muscle loss.

A landmark trial (NEJM 2020) showing that Dapagliflozin reduced kidney failure risk, eGFR decline of ≥50%, and death from renal or cardiovascular causes by 39% in CKD patients.

The EMPA-KIDNEY trial (NEJM 2023) confirmed that Empagliflozin reduced the risk of kidney disease progression or cardiovascular death by 28% down to an eGFR threshold of 20.

The CREDENCE trial (NEJM 2019) demonstrated that Canagliflozin reduced the risk of kidney failure by 30% in patients with type 2 diabetes and albuminuria.

These clinical trials demonstrated that Finerenone significantly reduces cardiorenal progression risk, including eGFR decline, kidney failure, and cardiovascular events in diabetic CKD.

CKDPartner provides educational clinical decision support based strictly on KDIGO 2024 guidelines and validated equations. It does not provide medical diagnosis or replace consulting a nephrologist.