(USMLE topics) Pathology, causes, symptoms, diagnosis and treatment of CKD.

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Chronic kidney disease, CKD, is a gradual loss of renal function, typically developing over the course of months or years. Many conditions, both within and outside the kidneys, can cause progressive damage to the kidneys over time, leading to CKD. Of these, most common are diabetes and hypertension, both of which directly damage blood vessels within the kidney, destroying renal tissue. An acute kidney injury, if not completely resolved, may also become chronic kidney disease.
The severity of renal disease is evaluated based on glomerular filtration rate, GFR, an indicator of how well the blood is filtered by the kidneys. GFR is calculated as a function of serum creatinine, a waste product that accumulates in blood plasma when renal function declines. The calculation takes into account the patient’s age, gender and race.
Symptoms develop slowly over time, progressing from renal insufficiency to endstage renal failure. Often, initial loss of renal tissue does not produce any symptoms, because the remaining healthy tissue becomes more active and can temporarily compensate for the loss, a phenomenon known as renal adaptation. Symptoms appear when a significant portion of kidney function is already lost. The ability to concentrate urine is usually the first to be impaired, resulting in frequent trips to the bathroom, especially at night. Other early signs include fatigue, loss of appetite, and decreased mental ability.
Because the kidneys remove metabolic wastes, control blood pH and fluid/electrolyte balance, as well as produce several hormones, loss of kidney function may result in a number of complications:
Accumulation of toxic nitrogenous wastes can cause a range of symptoms, from nausea, vomiting to confusion and seizures.
Reduced excretion of hydrogen ions leads to increased blood acidity, or metabolic acidosis.
Reduced excretion of potassium results in potassium overload in the blood, or hyperkalemia, which may cause cardiac arrhythmias. Hyperkalemia usually occurs only in advanced stage, but excessive potassium intake or use of drugs that prevent potassium excretion, may precipitate the condition in earlier stages.
Decreased excretion of phosphate results in hyperphosphatemia.
Reduced renal production of calcitriol, an active form of vitamin D, contributes to low blood calcium level, or hypocalcemia. Low blood calcium stimulates production of parathyroid hormone, PTH, by the parathyroid gland. PTH promotes calcium release from bones in an attempt to raise blood calcium. This sequence eventually leads to an overactive parathyroid gland, or secondary hyperparathyroidism, which can develop before hypocalcemia occurs. As the bones continuously lose calcium to the blood, they become thin and weakened, a condition known as renal osteodystrophy. Symptoms include bone and joint pain, and increased risks of fractures.
Reduced renal secretion of erythropoietin, a stimulating factor for red blood cell formation, can lead to anemia.
Diagnosis is based on renal function tests, which include blood and urine analysis. Ultrasound is performed to detect renal obstruction. It may also help in distinguishing chronic kidney disease from acute kidney injury based on kidney size.
Treatments aim to control the underlying condition, address the complications, and involve certain nutrition supplements and restrictions. Endstage kidney disease requires dialysis or kidney transplantation.