How the kidney controls fluid, electrolytes and acid–base balance

Reabsorption alone would leave urine roughly as concentrated as blood. To make urine several times more concentrated, or several times more dilute, the nephron uses an arrangement called the countercurrent multiplier. The loop of Henle dips deep into the medulla of the kidney, the inner zone around the renal pelvis that the rest of the nephron does not enter. Its descending limb is permeable to water but not to salt, so as fluid descends into the salty medulla, water leaves by osmosis and the fluid inside becomes more concentrated. Its ascending limb is the opposite — impermeable to water but actively pumping sodium and chloride out — so the fluid becomes dilute as it climbs, while the pumped salt builds and maintains the medullary gradient. Because the two limbs run side by side in opposite directions, each pass amplifies the gradient rather than washing it out. The vasa recta, hairpin capillaries that follow the loop, carry the reabsorbed water away without destroying the gradient. The result is a medulla that becomes progressively saltier toward the papilla, creating the osmotic force that can pull water out of the collecting duct.

Whether that force is used depends on vasopressin, also called antidiuretic hormone, released from the posterior pituitary. Vasopressin inserts water channels called aquaporin-2 into the collecting duct wall, so water follows the gradient back into the blood and a small volume of concentrated urine is produced. When vasopressin is suppressed, the channels are withdrawn, the collecting duct stays watertight, and a large volume of dilute urine is passed. A second hormone, aldosterone from the adrenal cortex, acts further upstream in the distal tubule, where it increases sodium reabsorption and potassium secretion; because water follows the reabsorbed sodium, aldosterone effectively expands the circulating volume. Aldosterone is the final step of the renin–angiotensin–aldosterone system: low renal perfusion pressure, low sodium delivery or sympathetic stimulation makes the kidney release renin, which converts angiotensinogen to angiotensin I, which angiotensin-converting enzyme converts to angiotensin II, a potent vasoconstrictor that also triggers aldosterone release.

Clinically these pieces explain concrete findings. A patient with a high vasopressin level, as in the syndrome of inappropriate antidiuretic hormone secretion, retains water and becomes hyponatraemic with concentrated urine. A patient with no vasopressin, as in cranial diabetes insipidus, passes many litres of dilute urine and becomes hypernatraemic if fluids are withheld. A patient on a loop diuretic has that medullary gradient itself dismantled, which is why loop diuretics are powerful and also why they waste potassium and can disturb calcium and magnesium handling.

Because the kidney sets the composition of body fluids, the laboratory report is really a report on the tubule. A useful approach is to read four things together rather than one at a time. First, the effective circulating volume: daily weight, intake and output, pulse, blood pressure, mucous membranes and skin turgor. Second, the sodium concentration, normally about 135 to 145 mmol/L. Sodium is not a measure of how much salt the body holds but of how much water dilutes it. A low sodium usually means relatively too much water, which can happen with heart failure, liver disease, or inappropriate vasopressin, and not only with salt loss. A high sodium almost always means a water deficit relative to salt.

Third, potassium, normally about 3.5 to 5.0 mmol/L. Potassium matters out of proportion to its number because it governs the resting electrical potential of every cell, especially cardiac muscle: a low value causes weakness, cramps and arrhythmias, while a high value causes muscle weakness, paraesthesia and, above roughly 6.5 mmol/L, classic electrocardiogram changes — tall peaked T waves, then a widened QRS, then a sine-wave pattern that precedes cardiac arrest. Fourth, the acid–base picture, usually read from a blood gas, with bicarbonate normally about 22 to 26 mmol/L and arterial pH about 7.35 to 7.40. The bicarbonate tells you the metabolic side and the carbon dioxide the respiratory side; the two normally move in opposite directions as compensation. When the bicarbonate is low with a low pH, the patient has metabolic acidosis, and the cause is found by considering the anion gap, the difference between measured cations and anions. A normal-gap acidosis, as in diarrhoea, is bicarbonate lost from the gut. A raised-gap acidosis, as in lactic acidosis, ketoacidosis or advanced kidney failure, is acid added to the body. When the bicarbonate is high with a high pH, the patient has metabolic alkalosis, as in prolonged vomiting with loss of stomach acid.

Two quantitative rules are worth carrying to the bedside. The first is that urine output below about 0.5 mL per kilogram per hour in an adult is oliguria and needs explanation. The second is that a serum creatinine rise of as little as 26 micromol/L in 48 hours already meets the definition of acute kidney injury, because creatinine is a late and insensitive marker and the tubule has usually lost much of its reserve before the number moves. Finally, the concentration of the urine itself is informative: a dilute urine in a patient who looks dry suggests the tubule has lost its concentrating ability, whereas a concentrated urine in the same patient suggests the kidney is working hard to conserve.

Nursing monitoring of a renal patient is not a ritual of recording numbers; each number tests one of the kidney’s jobs, and the value of the measurement lies in the decision it triggers. Daily weight is the most sensitive bedside index of fluid balance because a litre of retained water weighs a kilogram, while oedema and even lung crepitations appear later. Strict intake and output, measured on every shift, detect a falling urine output before the blood chemistry changes, and the character of the urine — colour, cloudiness, sediment — points to concentration, infection or stones. Blood pressure is monitored because the kidney both controls it and is damaged by it, and because a rising pressure may be the first sign of fluid overload.

Serum potassium deserves specific attention because it is the electrolyte that kills without warning: the nurse must know which patients are at risk, including those in kidney failure, those on angiotensin-converting enzyme inhibitors, potassium-sparing diuretics or potassium supplements, and those with diabetes or metabolic acidosis. Because the electrocardiogram changes of hyperkalaemia progress in a predictable order, a patient with a suspiciously high potassium is placed on continuous cardiac monitoring while treatment is prepared. Fluid overload is recognised by weighing the patient, listening to the lung bases, checking jugular venous pressure and looking for pitting oedema, and it is treated by restricting fluid and sodium and by giving the prescribed diuretic at the time that best matches the patient’s pattern of urine production. Uraemia, the syndrome of retained waste products, produces a characteristic cluster the nurse charts: nausea and vomiting, anorexia, a metallic taste, itching, drowsiness, confusion and eventually a pericardial rub or seizure. Drug therapy is monitored differently in kidney disease because the kidney is the main elimination route for many drugs: doses are reduced, dosing intervals extended, and levels checked, and the nurse who gives an aminoglycoside or a renally cleared opioid without checking the renal function is creating the toxicity she will later have to report.

Patient education follows the same logic. The patient is taught which foods carry potassium and phosphate, why protein and sodium may be restricted, why fluid may be limited to a prescribed volume, how to recognise the warning symptoms of hyperkalaemia or fluid overload, and why every non-prescribed medicine, including herbal remedies and painkillers bought without prescription, must be checked with the health worker first. Finally, the nurse watches the access route: a fistula or a peritoneal dialysis catheter is the patient’s lifeline, so its thrill, bruit, cleanliness and the absence of pressure on that arm are assessed every shift, and any suspicion of infection or loss of function is escalated immediately rather than documented and left.