Last time we reviewed the proposed mechanisms by which hypercalcaemia can induce polyuria. It’s important to know that hypokalaemia can also precipitate this presentation. So here are the proposed mechanisms for this scenario.
Potassium is required for the thick ascending limb NaKCl2 co-transporter to operate. Remember that potassium is recycled via the apical ROMK channel, which facilitates ongoing sodium reabsorption in the TAL and maintenance of the medullary concentration gradient. Therefore, potassium deficiency may lead to concentrating defects via this pathway, leading to polyuria.
There is also some evidence that hypokalaemia leads to impaired responsiveness to ADH. The exact mechanism is unclear, but obviously decreased responsiveness to ADH may lead to large volumes of dilute urine.
Other interesting nuggets with hypokalaemia – movement of potassium out of cells in the proximal tubule (in the setting of hypokalaemia) is balanced by inward movement of hydrogen ions. The creation of an intracellular acidosis increases ammonia production by the proximal tubular cells, which may exacerbate problems in patients with decompensated liver disease.
Chronic potassium depletion (over a month at least) in humans can cause the development of vacuolar lesions in renal epithelial cells, primarily in the proximal tubule. If the deficiency persists over a longer time period, changes including interstitial nephritis, tubular atrophy and medullary cyst formation have been described. Potential mechanisms underlying these changes may be related to altered growth factor and cytokine production, or ammonia accumulation. This collection of findings has loosely been referred to as hypokalaemic nephropathy.