What is uremia?

People have a deep fear of uremia. So, what causes uremia? In fact, many people don’t understand this issue. However, medical research shows that knowing what causes uremia is actually very important for people's treatment process. In fact, many minor kidney diseases can become the cause of uremia, so people should treat kidney disease correctly. Let’s take a look at what uremia is.

Uremia is not an independent disease, but a clinical syndrome common to various advanced kidney diseases and the terminal stage of chronic renal failure.

Clinical manifestations

Disorders of water, electrolyte, acid and alkali metabolism

Metabolic acidosis and water and electrolyte imbalance are the most common.

(1) Metabolic acidosis During the uremic stage of chronic renal failure, the acidic products of human metabolism, such as phosphoric acid and sulfuric acid, are retained due to renal excretion disorders, which may cause "uremic acidosis". In mild chronic acidosis, most patients have fewer symptoms, but if arterial blood HCO3 <15 mmol/L, they may experience obvious loss of appetite, vomiting, weakness, deep breathing, etc.

(2) Disorders of water and sodium metabolism, mainly manifested as water and sodium retention, or hypovolemia and hyponatremia. In renal insufficiency, the kidney's ability to adapt to excessive sodium load or excessive volume gradually decreases. If patients with uremia do not restrict water appropriately, it may lead to excessive volume load, with varying degrees of subcutaneous edema (eyelids, lower limbs) and/or body cavity effusion (thoracic cavity, abdominal cavity). At this time, they are prone to high blood pressure, left ventricular failure (manifested as chest tightness, decreased activity tolerance, and even inability to lie flat at night) and cerebral edema. On the other hand, when the patient has a large amount of urine but excessively restricts water intake, or has concurrent gastrointestinal symptoms such as vomiting and diarrhea, dehydration can easily occur. In clinical practice, excessive volume load is more common. Therefore, patients with uremia should pay attention to properly controlling their water intake (in addition to drinking water, it also includes soup, porridge, fruit and other water-rich foods). Excessive fluid replacement should be avoided during diagnosis and treatment to prevent heart failure and pulmonary edema.

(3) Potassium metabolism disorder: When GFR drops to 20-25 ml/min or lower, the kidney's ability to excrete potassium gradually decreases, and hyperkalemia is prone to occur at this time; especially when excessive potassium intake, acidosis, infection, trauma, gastrointestinal bleeding, etc. occur, hyperkalemia is more likely to occur. Severe hyperkalemia (serum potassium > 6.5 mmol/L) is dangerous and requires prompt treatment (see Treatment of Hyperkalemia). Hypokalemia may sometimes occur due to insufficient potassium intake, excessive gastrointestinal loss, the use of potassium-excreting diuretics and other factors. Hyperkalemia is the most common clinical condition, so patients with uremia should strictly limit their intake of high-potassium foods and have their blood potassium checked regularly.

(4) Calcium-phosphorus metabolism disorder, mainly manifested as excess phosphorus and calcium deficiency. In chronic renal failure, the kidneys produce less 1,25-(OH)2D3, which reduces intestinal absorption of calcium; the target organs develop resistance to 1,25-(OH)2D3, which reduces calcium reabsorption by the renal tubules. In addition, hyperphosphatemia can increase the calcium-phosphorus product, promote the deposition of calcium phosphates, cause ectopic calcification, and decrease blood calcium. Food is rich in phosphorus, and blood phosphorus concentration is regulated by intestinal absorption of phosphorus and kidney excretion. When the glomerular filtration rate decreases and urinary phosphorus excretion decreases, the blood phosphorus concentration gradually increases. High blood phosphorus further inhibits the synthesis of 1,25-(OH)2D3 and aggravates hypocalcemia. The parathyroid glands compensate by secreting more PTH to maintain blood calcium. Leading to secondary hyperparathyroidism (abbreviated as hyperparathyroidism).