Is back pain caused by uremia?

Uremia is a comprehensive disease. It does not simply refer to a certain disease. It includes the disorders and degeneration of functions of the cardiovascular, intestinal, and endocrine systems. It may also cause complications such as high blood pressure and anemia. Once contracted, the disease is very difficult to treat. If you experience lower back pain, you may have uremia. However, there are many causes of low back pain, and a comprehensive assessment should be made based on other symptoms.

Chronic renal failure refers to a clinical syndrome consisting of a series of symptoms and metabolic disorders caused by various kidney diseases that lead to progressive and irreversible decline in renal function until loss of function. It is referred to as chronic renal failure. The end stage of chronic renal failure is commonly known as uremia. Uremia is not an independent disease, but a clinical syndrome common to various advanced kidney diseases. It is a syndrome composed of a series of clinical manifestations that appear when chronic renal failure enters the terminal stage.

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).

Metabolic disorders of proteins, carbohydrates, fats and vitamins

Protein metabolism disorders in CRF patients are generally manifested as accumulation of protein metabolites (azotemia), including urea, guanidine compounds, creatinine, amines, indoles, phenols and middle-molecular substances.

Urea is excreted through the kidneys. Urea accumulates in the body in uremia, which may be associated with symptoms such as fatigue, anorexia, vomiting, inattention, low body temperature, and bleeding tendency. Guanidine compounds: Under normal circumstances, arginine is mainly metabolized in the liver into urea, guanidineacetic acid, and creatinine. Urea and creatinine accumulate in uremia, while arginine can be broken down into methylguanidine and guanidinoarginine through other pathways. Among them, methylguanidine is the most toxic small molecule, and its accumulation in the body can reach 70 to 80 times the normal value. It is associated with many clinical symptoms such as weight loss, shortened red blood cell life, vomiting, diarrhea, and drowsiness. Amines: Aliphatic amines can cause myoclonus, flapping tremors and hemolysis; polyamines (spermine, cadaverine, putrescine) can cause anorexia, nausea, vomiting and proteinuria, and can promote red blood cell lysis, inhibit the production of erythropoietin, and promote the occurrence of pulmonary edema, ascites and cerebral edema in renal failure.