Acidosis & Electrolytes

By the end of this chapter you should be able to:

• Explain why metabolic acidosis develops in CKD and the harm it causes to bone, muscle, potassium, and progression.
• Treat metabolic acidosis with oral bicarbonate to an appropriate target, avoiding over-correction.
• Summarise the evidence on bicarbonate for slowing progression and its limits.
• Explain why hyperkalaemia develops in CKD and is worsened by the progression-slowing pillars.
• Manage chronic hyperkalaemia so that RAAS blockade and finerenone can continue.
• Use potassium binders appropriately and know which agent to avoid.
• Manage magnesium and avoid magnesium-containing agents in advanced CKD.
• Decide when to treat hyperuricaemia, and recognise that urate-lowering does not slow CKD progression.

• As nephrons are lost, the kidney excretes less acid, and a metabolic acidosis develops — initially normal-anion-gap, then high-anion-gap in advanced disease.
• Acidosis is not benign: it buffers acid in bone (worsening CKD-MBD), drives muscle protein catabolism and wasting, aggravates hyperkalaemia, and accelerates CKD progression.
• Treat with oral sodium bicarbonate to keep the serum bicarbonate at or above about 22, without over-correcting into alkalosis or excess sodium and volume.
• Some trials show bicarbonate slows progression and preserves nutrition, while others, including in the elderly, are neutral — so the benefit is plausible but not uniform.
• A base-rich, plant-dominant diet lowers the acid load and is a complementary approach.
• Hyperkalaemia arises from reduced renal potassium excretion and is worsened by RAAS blockade and finerenone, acidosis, constipation, and diet.
• Severe hyperkalaemia with ECG changes is an emergency treated with the standard measures; the CKD-specific challenge is chronic management.
• The goal of chronic management is to keep patients on the protective pillars, not to stop them at the first elevated potassium.
• Restrict dietary potassium thoughtfully, correct acidosis, use diuretics, and add a modern potassium binder — patiromer or sodium zirconium cyclosilicate — to enable continued RAAS blockade.
• Avoid sodium polystyrene sulfonate where modern binders are available, given its gastrointestinal risk.
• Magnesium accumulates as excretion falls, so avoid magnesium-containing laxatives and antacids in advanced CKD.
• Hyperuricaemia is common, but urate-lowering does not slow CKD progression — treat symptomatic gout, not asymptomatic hyperuricaemia, for renoprotection.
• Correcting acidosis and managing potassium are, in part, ways of protecting the bone, the muscle, and the pillars — not isolated number-chasing.

The failing kidney loses control of the body's chemistry, and two disturbances in particular are both common and actionable: metabolic acidosis and hyperkalaemia. Each is more than a number on a panel. Acidosis quietly erodes bone and muscle and may hasten the kidney's own decline; hyperkalaemia is the side effect that most often drives clinicians to abandon the very drugs that protect the kidney. Managing both well is less about chasing values than about protecting the patient and preserving the therapies of Part 2.

Why acidosis develops, and why it matters

The kidney's job in acid-base balance is to excrete the daily acid load, largely by generating ammonia in the tubule. As nephrons are lost, ammoniagenesis and acid excretion fall, and acid accumulates — a metabolic acidosis that begins as a normal-anion-gap picture and, in advanced CKD, acquires a high anion gap as retained anions build up. The reason to treat it is that acidosis is not inert. The body buffers the retained acid in bone, demineralising it and worsening the mineral-bone disorder of the last chapter. It drives muscle protein catabolism, contributing to the protein-energy wasting that harms CKD patients. It aggravates hyperkalaemia by shifting potassium out of cells. And it appears to accelerate CKD progression itself, acting as one of the amplifiers of Chapter 2 through ammonia-mediated and hormonal tubular injury. So correcting acidosis is, simultaneously, a bone, muscle, potassium, and progression intervention.

Treating acidosis with bicarbonate

The mainstay is oral sodium bicarbonate, titrated to keep the serum bicarbonate at or above about 22 mmol/L. The aim is correction, not over-correction: pushing bicarbonate above the normal range courts a metabolic alkalosis and, because bicarbonate is a sodium salt, adds a sodium and volume load that can worsen blood pressure, so the target is the lower-normal range rather than the highest achievable. The evidence is genuinely mixed. Some trials — including an influential one — found that correcting acidosis slowed CKD progression and preserved nutritional status, while others, particularly in older patients, were neutral on the outcomes they measured. The honest reading is that bicarbonate is plausibly progression-slowing and clearly corrects a harmful metabolic state, but the magnitude of the progression benefit is uncertain. A base-rich, plant-dominant diet, which lowers the dietary acid load, is a complementary and increasingly favoured approach, and newer acid-binding agents are under investigation. Correct the acidosis; do not over-correct it.

Why hyperkalaemia is the pillar-limiting problem

Potassium excretion depends on functioning nephrons and on aldosterone, both compromised in CKD, so hyperkalaemia is common and becomes more so as the GFR falls. Several factors stack on top: the RAAS blockade and finerenone of Part 2 reduce aldosterone-driven potassium excretion and raise potassium; acidosis shifts potassium out of cells; constipation reduces the colonic excretion that becomes important in CKD; and a high-potassium diet adds load. The clinical importance is specific. Severe hyperkalaemia with ECG changes is an acute emergency managed with the standard measures — calcium to stabilise the membrane, insulin-glucose and other shifts, and removal — covered with the electrolyte emergencies elsewhere. But the CKD-defining problem is chronic hyperkalaemia, and its significance is that it is the commonest reason clinicians stop RAAS blockade and finerenone, forfeiting the kidney and cardiovascular protection those drugs provide. Managing chronic hyperkalaemia is, in large part, about keeping patients on the pillars.

Managing chronic hyperkalaemia

The chronic-management toolkit is built to enable, not abandon, the protective drugs. Dietary potassium is restricted thoughtfully — mindful of the potassium paradox of Chapter 6, where a healthy plant-rich diet is potassium-rich but beneficial, so blanket restriction is avoided. Acidosis is corrected, which itself lowers potassium. Diuretics enhance renal potassium excretion. Constipation is treated. And the modern potassium binders — patiromer and sodium zirconium cyclosilicate — bind potassium in the gut and have transformed chronic management by allowing RAAS blockade and finerenone to be continued at effective doses rather than withdrawn. The older binder, sodium polystyrene sulfonate, is best avoided where the modern agents are available, given concern about gastrointestinal injury including bowel necrosis. The governing principle, carried from the RAAS chapter, is to manage the potassium so the drug can stay, reserving discontinuation for hyperkalaemia that genuinely cannot be controlled.

Magnesium, urate, and the other electrolytes

Two further electrolyte issues deserve brief, specific attention. Magnesium is excreted by the kidney, so as the GFR falls magnesium accumulates, and the practical lesson is to avoid magnesium-containing laxatives and antacids in advanced CKD, which can precipitate dangerous hypermagnesaemia. Hyperuricaemia is common in CKD and tempts clinicians to treat it for renoprotection, but the trials of urate-lowering therapy in CKD did not show a slowing of progression — so urate-lowering is indicated for symptomatic gout, which is genuinely more frequent in CKD, but not for asymptomatic hyperuricaemia in the hope of protecting the kidney. The other disturbances — sodium and water handling, phosphate (the subject of the mineral-bone chapter) — are managed in their own contexts; the CKD-specific, high-yield actions of this chapter are correcting acidosis and managing potassium.

Where the evidence is firm, and where it is mixed

The firm parts are mechanistic and practical: that acidosis harms bone, muscle, and potassium balance, that potassium binders enable continuation of RAAS blockade, and that urate-lowering does not slow CKD progression are all well supported, the last by dedicated randomised trials. The mixed part is the progression benefit of bicarbonate — promising in some trials, neutral in others — so it is treated as a reasonable, low-risk intervention that corrects a harmful state, rather than a proven disease-modifier on the level of the Part-2 pillars. The disciplined approach is to correct acidosis without over-correcting, to use binders to keep patients on their protective drugs, to avoid magnesium loading, and to spare patients urate-lowering therapy given for the wrong reason.

Table 9.1 — Metabolic acidosis in CKD

Table 9.2 — Bicarbonate therapy: evidence and cautions

Table 9.3 — Causes of hyperkalaemia in CKD

Table 9.4 — Managing chronic hyperkalaemia

Table 9.5 — Magnesium and urate in CKD

Table 9.6 — The acidosis–progression–pillar links

Visualise & Map

Clinical Reasoning

Safety & Evidence

Panel A — Red flags

Panel B — Never do

Pitfall 1 — Ignoring the acidosis

Pitfall 2 — Over-correcting

Pitfall 3 — Stopping the pillar

Pitfall 4 — The old binder

Pitfall 5 — Treating the urate number

Graded statements (by evidence type)

Patient Decisions

Natural-frequency estimates for orientation, from the relevant trials; they vary with population and severity. They convey the size of the acidosis and potassium decisions, expressed per 100 comparable patients.

Apply & Test

Paste-ready notes. Tick the boxes that apply and delete the rest; make the bicarbonate target and the pillar-preservation explicit.

Template 1 — Acidosis and bicarbonate plan

• Serum bicarbonate ___ ; anion gap ___ — ☐ normal-gap ☐ high-gap (advanced).
• Harms noted: ☐ bone (Chapter 8) ☐ muscle/wasting ☐ hyperkalaemia ☐ progression.
• Oral bicarbonate started/titrated to keep ≥ 22; ☐ NOT over-corrected (target lower-normal ~22–26).
• Base-rich/plant-dominant diet considered: ☐ yes.
• Monitoring: bicarbonate, sodium, volume, BP.

Template 2 — Chronic hyperkalaemia management

• Potassium ___ — ☐ acute/ECG changes → emergency management ☐ chronic.
• Contributors addressed: ☐ acidosis corrected ☐ constipation treated ☐ diuretic optimised ☐ diet (mind potassium paradox).
• Binder: ☐ patiromer ☐ sodium zirconium cyclosilicate (SPS avoided).
• Protective pillars: ☐ RAAS blockade continued ☐ finerenone continued (not reflexively stopped).
• Magnesium: ☐ Mg-containing laxatives/antacids avoided.
• Urate: ☐ treat only symptomatic gout (not asymptomatic for renoprotection).