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PH-RN02

Chronic kidney disease

How losing nephrons makes the survivors overwork and scar, and how failing kidneys cause high blood pressure, acidosis, anaemia and disordered bone and mineral balance.

By the end, you can

  • Describe the excretory and endocrine roles of the healthy kidney.
  • Explain how hyperfiltration in surviving nephrons can drive further glomerulosclerosis and interstitial fibrosis.
  • Relate the loss of nephrons to hypertension, metabolic acidosis and nocturia.
  • Explain why chronic kidney disease causes anaemia and secondary hyperparathyroidism.
  • Recognise the appearance of the end-stage kidney, the KDIGO GFR and albuminuria categories and the main tests, and explain how each main treatment acts on the mechanism.

What it is

Chronic kidney disease (CKD) is an abnormality of kidney structure or function present for more than three months, shown by a reduced glomerular filtration rate, by markers of damage such as albuminuria, or both. It is staged by GFR and by albuminuria; diabetes and hypertension are the commonest causes.

Normal function

Many nephrons, several jobs

Each kidney holds roughly a million nephrons, though the number varies widely between people. Each filters a little plasma and the beyond it reclaims what the body needs. Together they give a GFR of about 120 mL/min, with spare capacity: one healthy kidney can keep blood creatinine normal.

The kidneys balance salt and water, which helps set blood pressure, and excrete potassium, phosphate and acid, making new bicarbonate as they do. They are also endocrine organs: fibroblast-like cells between the cortical tubules release erythropoietin (EPO) when oxygen delivery falls, and proximal tubule cells convert vitamin D to its active form, calcitriol.

Adult kidneys cannot make new nephrons, so a nephron that is lost is not replaced.

Point to it on the model