Acid-base disorders · KIMS Secunderabad
Metabolic Acidosis — When Blood pH Falls and Why Kidneys Are at the Centre
Metabolic acidosis is a reduction in blood pH (below 7.35) caused by an excess of acids or a loss of bicarbonate, with a compensatory fall in arterial PCO2 as the respiratory system attempts to partially correct the pH by increasing the rate and depth of breathing (Kussmaul respirations — deep, rapid breathing in severe metabolic acidosis). The kidneys are central to acid-base regulation — they excrete the daily metabolic acid load (approximately 50 to 100 mEq/day of hydrogen ions) and regenerate bicarbonate. When the kidneys fail — in CKD, AKI, or specific tubular disorders — metabolic acidosis is one of the most consistent and clinically significant complications.
Metabolic acidosis is not a diagnosis — it is a laboratory finding that points toward an underlying cause requiring identification and treatment. The anion gap calculation is the essential first step in identifying the cause: it distinguishes between acidosis caused by accumulation of unmeasured anions (high anion gap) and acidosis caused by bicarbonate loss with compensatory chloride retention (normal anion gap, hyperchloraemic acidosis).
The anion gap — the essential classification tool
Anion gap (AG) = serum sodium − (serum chloride + serum bicarbonate). Normal = 8 to 12 mEq/L. The AG represents unmeasured anions (albumin, phosphate, lactate, ketones, uraemic organic acids) that are not measured in the standard electrolyte panel. When pathological anions accumulate (lactic acid, ketoacids, uraemic toxins, ingested toxic alcohols), the AG rises while sodium and chloride remain unchanged — high anion gap metabolic acidosis. When bicarbonate is lost (from the gut or kidneys) and chloride rises to maintain electroneutrality, the AG remains normal — normal anion gap (hyperchloraemic) metabolic acidosis.
High anion gap metabolic acidosis · AG above 12 mEq/L
Lactic acidosis (sepsis — most common cause of HAGMA in ICU, shock, mesenteric ischaemia, liver failure, metformin toxicity) · Diabetic ketoacidosis (DKA — absent or low insulin, hyperglycaemia, ketones) · Uraemic acidosis (advanced CKD or AKI — retained uraemic organic acids) · Toxic alcohol ingestion (methanol, ethylene glycol — extremely high AG) · Salicylate toxicity. Treatment: treat the underlying cause (antibiotics/source control for sepsis, insulin for DKA, dialysis for uraemia, antidotes for toxic alcohols).
Normal anion gap metabolic acidosis · AG 8–12 mEq/L (hyperchloraemic)
Renal tubular acidosis (Type 1, 2, or 4) · Diarrhoea (most common cause of NAGMA in India — intestinal bicarbonate loss) · Post-ileostomy or short bowel · Ureteral diversion (ureterosigmoidostomy — bowel reabsorbs urinary chloride and excretes bicarbonate) · Dilutional acidosis from large volume 0.9% saline infusion. Treatment: oral sodium bicarbonate or potassium citrate · treat the diarrhoea · modify the urinary diversion.
Metabolic acidosis in CKD — the most common chronic cause
As eGFR declines below 25 to 30 ml/min, the remaining nephrons cannot excrete the daily acid load — uraemic organic acids and, importantly, ammonium excretion capacity is reduced (ammonium is the primary vehicle for acid excretion in the urine). The result is a normal or mildly elevated anion gap metabolic acidosis that is chronic, persistent, and — critically — actively accelerates CKD progression:
Acidosis stimulates the complement system and promotes tubulointerstitial inflammation and fibrosis — directly worsening CKD.
Acidosis stimulates muscle protein catabolism — releasing glutamine as a buffering substrate, causing progressive sarcopenia.
Acidosis accelerates bone mineral loss — acid is buffered by calcium carbonate released from bone.
Acidosis impairs insulin sensitivity and worsens glucose control in diabetic CKD patients.
The BICARBONATE trial and multiple observational studies show that oral sodium bicarbonate supplementation in CKD patients with serum bicarbonate below 22 mEq/L slows eGFR decline compared to placebo — making bicarbonate supplementation one of the few cheap, simple, effective kidney-protective interventions that is still underused in practice.
Treatment at KIMS
Oral sodium bicarbonate — for CKD-related chronic metabolic acidosis
Target serum bicarbonate above 22 mEq/L (and ideally 23 to 25 mEq/L). Starting dose: 650mg tablets (approximately 8 mEq bicarbonate) twice daily, titrated to the serum bicarbonate response. Side effects: bloating, sodium load (avoid in volume-overloaded or hypertensive patients not tolerating sodium). Potassium citrate is preferred in patients with concurrent hypokalaemia and Type 1 or 2 RTA (provides alkali + potassium + citrate).
IV sodium bicarbonate — for acute severe metabolic acidosis
pH below 7.1 or bicarbonate below 10 mEq/L in AKI or severe lactic acidosis. The decision to use IV bicarbonate in lactic acidosis is nuanced — studies show no benefit for lactic acidosis from sepsis above pH 7.15 (the standard BICARB-ICU trial result). However, bicarbonate is beneficial for AKI-related acidosis in patients not yet on dialysis, and in specific situations (severe hyperkalaemia with acidosis — bicarbonate shifts potassium into cells and corrects the acidosis simultaneously). IV bicarbonate given too rapidly causes paradoxical intracellular acidosis, hypocalcaemia, and sodium overload — it is given slowly over 4 to 6 hours.
CRRT with bicarbonate-buffered replacement fluid — for severe acidosis requiring dialysis
In patients with AKI and severe metabolic acidosis (pH below 7.1, bicarbonate below 8 mEq/L) who are haemodynamically unstable, CRRT with bicarbonate-based replacement and dialysate fluid provides continuous acid-base correction. Available 24/7 at KIMS ICU.
Book a Nephrology Assessment for Metabolic Acidosis at KIMS. Call 040-4488-5000
Frequently Asked Questions — Metabolic Acidosis
Blood pH is normally 7.35 to 7.45 — slightly alkaline. Acidosis means the pH has fallen below 7.35. At this level, cellular enzyme function is impaired — most enzymes work optimally near neutral pH and progressively lose function as pH falls. The consequences of severe acidosis: reduced cardiac contractility (the heart pumps less effectively), insulin resistance (glucose cannot be metabolised efficiently), impaired clotting, altered drug binding to proteins (affecting drug distribution and metabolism), and CNS depression (confusion, coma in severe cases). At pH below 7.1 — severe acidosis — the risk of cardiac arrhythmia and circulatory collapse is high.
The anion gap is a calculated number — serum sodium minus (serum chloride + serum bicarbonate) — that estimates the unmeasured negatively charged ions (anions) in the blood. Normal is 8 to 12 mEq/L. When abnormal acids accumulate (lactic acid, ketoacids, uraemic toxins, toxic alcohols), the anion gap rises because these acids are not measured in the standard electrolyte panel. This high AG points toward one of the serious acute causes of acidosis. A normal AG with low bicarbonate points toward bicarbonate loss — from the gut (diarrhoea — the most common in India) or the kidneys (renal tubular acidosis). The AG distinguishes these two categories, which have very different causes and treatments.
Yes — and they should, if their serum bicarbonate is persistently below 22 mEq/L. Oral sodium bicarbonate tablets (650mg, approximately 8 mEq bicarbonate) are safe, inexpensive, and effective for CKD-related metabolic acidosis. The main concerns: sodium content (each 650mg tablet provides approximately 180mg of sodium — relevant in volume-overloaded or hypertensive patients), bloating and belching (from CO2 released in the stomach), and the need to take tablets regularly (compliance). At KIMS, serum bicarbonate is checked at every CKD clinic visit and bicarbonate supplementation is started when it falls below 22 mEq/L.
Lactic acidosis is a high anion gap metabolic acidosis caused by the accumulation of lactic acid — produced when cells are forced into anaerobic metabolism (without oxygen). The most common cause is tissue hypoperfusion from septic shock, cardiogenic shock, or haemorrhagic shock — cells cannot receive adequate oxygen and switch to lactic acid production. Other causes: liver failure (the liver normally clears lactate from the bloodstream — failure allows it to accumulate), metformin in the setting of AKI or severe liver disease (metformin inhibits hepatic lactate metabolism), and severe respiratory failure. Lactic acidosis has a blood lactate above 5 mmol/L with pH below 7.35. Treatment is directed at the cause — fluid resuscitation and vasopressors for septic shock, stopping metformin, treating liver failure.
KIMS Secunderabad — Dr. E. Ravi (Senior Consultant Nephrologist, critical care nephrology), arterial blood gas analysis, anion gap calculation, serum lactate, urine anion gap for RTA diagnosis, IV bicarbonate protocols, CRRT with bicarbonate-buffered replacement fluid for severe acidosis, oral sodium bicarbonate and potassium citrate for CKD-related acidosis, BICARB protocol. NABH and NABL accredited. Emergency line: 040-4488-5000.