Hyperchloraemia and Hypochloraemia

Also known as: Hyperchloremia, Hypochloremia, Chloride disorders

Chloride is the principal extracellular anion and moves largely in parallel with sodium and inversely with bicarbonate.

Chloride abnormalities are rarely a primary problem in their own right; their value is as a pointer to the underlying disorder, particularly in acid-base interpretation, where the chloride level distinguishes normal anion gap from raised anion gap acidosis.

Hyperchloraemia occurs with large-volume 0.9% saline administration (which contains 154 mmol/L of chloride, well above physiological), gastrointestinal bicarbonate loss from diarrhoea, renal tubular acidosis, carbonic anhydrase inhibitors, and dehydration with water loss exceeding solute loss.

Hypochloraemia occurs with vomiting or nasogastric aspiration (loss of gastric hydrochloric acid), loop and thiazide diuretics, and any cause of metabolic alkalosis, alongside dilutional causes such as SIADH and heart failure.

Chloride should always be interpreted alongside sodium, bicarbonate and the anion gap rather than in isolation, since the same chloride value carries different meaning at different sodium levels
Calculate the anion gap: Na − (Cl + HCO₃). A raised chloride with a normal anion gap and low bicarbonate indicates a hyperchloraemic (normal anion gap) metabolic acidosis
The chloride-to-sodium ratio is a useful refinement, since it corrects for changes in free water and identifies chloride excess or deficit that the absolute value obscures
Urine chloride is the more informative test in metabolic alkalosis, distinguishing saline-responsive causes (urine chloride low, typically under 20 mmol/L — vomiting, nasogastric loss, prior diuretic use) from saline-resistant causes (urine chloride high: hyperaldosteronism, current diuretic use, Bartter and Gitelman syndromes).
Urine sodium is unreliable for this purpose in alkalosis, because bicarbonate excretion obligates sodium loss
Review fluid prescriptions and drug charts, since iatrogenic causes dominate hyperchloraemia in hospital practice
Venous blood gas gives chloride and bicarbonate together for rapid assessment

Management is directed at the underlying disorder rather than at the chloride value itself.

Hyperchloraemia:

Reduce or stop the chloride load: switch from 0.9% saline to a balanced crystalloid such as Hartmann's or Plasma-Lyte, which have a chloride content closer to plasma and produce less acidosis in large-volume resuscitation
Treat gastrointestinal losses and the underlying cause of diarrhoea
Address renal tubular acidosis where identified
Bicarbonate replacement is reserved for severe or symptomatic acidosis rather than used to normalise a number

Hypochloraemia:

Chloride-containing fluid replacement, usually as 0.9% saline, which is the correct choice here precisely because of its chloride content
Potassium chloride where hypokalaemia coexists, which it usually does in vomiting and diuretic-related cases
Treat the cause: antiemetics and management of gastric outlet obstruction where relevant, review of diuretic dosing, and investigation for hyperaldosteronism in saline-resistant cases
In diuretic-induced hypochloraemic alkalosis, acetazolamide is sometimes used, and potassium-sparing agents may reduce ongoing loss

Referral: nephrology for renal tubular acidosis, unexplained persistent chloride disturbance, or suspected Bartter or Gitelman syndrome; endocrinology if hyperaldosteronism is suspected.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Chronic Kidney Disease

Also known as: CKD, Chronic renal failure

Chronic kidney disease is abnormal kidney structure or function present for more than three months, with implications for health.

It is classified by cause, GFR category (G1–G5) and albuminuria category (A1–A3) — the "CGA" system — because albuminuria independently predicts progression and cardiovascular risk, and staging on GFR alone substantially underestimates risk in a patient with heavy proteinuria.

G1: GFR ≥90 with evidence of kidney damage; G2: 60–89; G3a: 45–59; G3b: 30–44; G4: 15–29; G5: below 15 (kidney failure)
A1: ACR below 3 mg/mmol; A2: 3–30; A3: above 30

The commonest causes are diabetes and hypertension, followed by glomerulonephritis, polycystic kidney disease, obstructive uropathy and recurrent pyelonephritis. Most patients with chronic kidney disease die of cardiovascular disease rather than reaching dialysis, which is why cardiovascular risk management is not a secondary consideration but a central part of treatment.

eGFR and urine albumin-to-creatinine ratio, both required for staging, and both confirmed on repeat over at least three months to establish chronicity and to distinguish from acute kidney injury
Urinalysis for haematuria and proteinuria; the combination of haematuria and proteinuria suggests glomerular disease and warrants nephrology referral
Renal ultrasound to assess size, symmetry and obstruction; small echogenic kidneys support chronicity, while asymmetry suggests renovascular disease and normal-sized kidneys in advanced disease suggest diabetes, amyloid or polycystic disease
Cause-directed investigations: HbA1c, blood pressure, autoimmune screen, myeloma screen in older patients with unexplained disease, hepatitis and HIV serology where relevant
Complication screening, which should be systematic: FBC for anaemia, calcium, phosphate, PTH and vitamin D for mineral and bone disorder, bicarbonate for metabolic acidosis, potassium, and lipids
Track the rate of decline rather than single values; a rapid fall (more than 5 mL/min/1.73m² per year) changes management and prompts referral
Medication review at every visit, since nephrotoxins and inappropriately dosed drugs are a major modifiable cause of progression

Slowing progression, which is the central goal:

Blood pressure control, generally targeting below 130/80 mmHg where tolerated, and lower in significant proteinuria
ACE inhibitor or ARB for proteinuric chronic kidney disease and for diabetic kidney disease, titrated to the maximum tolerated dose. Expect a creatinine rise of up to 25–30% after initiation, which is acceptable and reflects the intended haemodynamic effect; a larger rise warrants investigation for renovascular disease
SGLT2 inhibitors are now a cornerstone of treatment, with clear benefit in slowing progression in both diabetic and non-diabetic chronic kidney disease, and additional cardiovascular and heart failure benefit
Glycaemic control in diabetes, with agent selection accounting for renal clearance
Finerenone for diabetic kidney disease with albuminuria, as an additional option
Dietary sodium restriction, smoking cessation, weight management and exercise
Avoid nephrotoxins: NSAIDs, unnecessary contrast, aminoglycosides; adjust drug doses for renal function and provide sick-day guidance for holding ACE inhibitors, ARBs, diuretics, metformin and SGLT2 inhibitors during acute illness

Managing complications:

Anaemia: iron studies first and iron replacement before considering erythropoiesis-stimulating agents, targeting a haemoglobin around 100–120 g/L rather than normalising it, since higher targets increase cardiovascular events
Mineral and bone disorder: dietary phosphate restriction and phosphate binders taken with meals, activated vitamin D and calcimimetics for secondary hyperparathyroidism
Metabolic acidosis: oral sodium bicarbonate where bicarbonate is persistently below about 22 mmol/L, which slows progression and reduces muscle wasting
Hyperkalaemia: dietary advice, potassium binders where needed to allow continuation of prognostically important ACE inhibitors and ARBs rather than stopping them
Cardiovascular risk: statin therapy for essentially all patients, and active management of all modifiable risk factors

Advanced disease:

Timely nephrology referral — generally for G4 and above, rapid progression, heavy proteinuria, unexplained disease, refractory hypertension, or persistent haematuria — allowing planning rather than crisis management
Preparation for renal replacement therapy well before it is needed, including modality choice, dialysis access creation, and pre-emptive transplant assessment, which offers the best outcomes
Conservative kidney management is an appropriate and actively chosen pathway for frail or comorbid patients, focusing on symptom control and quality of life, and should be discussed rather than presented as the absence of treatment

Referral: nephrology per the criteria above; dietitian for phosphate, potassium and protein management; cardiology where cardiovascular disease coexists.

Hyperchloraemia and Hypochloraemia

Overview

Diagnosis

Management

Overview

Diagnosis

Management