Hypokalemic nephropathy

Introduction to hypokalemia nephropathy Hypokalmicnephropathy is a chronic interstitial nephritis or kidney disease caused by persistent hypokalemia, also known as kalium-losing nephropathy. The severity depends on the extent and duration of potassium deficiency. The clinical manifestations are mainly urinary concentrating dysfunction, but it is rare in clinical practice. basic knowledge The proportion of illness: 0.001% Susceptible people: no specific people Mode of infection: non-infectious Complications: pyelonephritis

Causes of hypokalemia nephropathy

(1) Causes of the disease

The disease is caused by chronic hypokalemia, the cause of hypokalemia is mainly due to insufficient potassium intake; excessive loss (digestive tract loss and loss of urine), various diuretics and steroids Hormone application; chronic kidney disease such as renal tubular acidosis, Bartter syndrome, Liddle syndrome, renin secretory tumor, Cushing's syndrome and hydroxylase deficiency disease, etc. Clinically common hypokalemia:

1. Non-nephrogenic hypokalemia The potassium excretion of the kidneys has not increased. The increase of potassium intake in cells due to various reasons is also one of the common causes of hypokalemia. The hypokalemia caused by the increase of potassium in the cells is mostly temporary. In most cases, no special treatment is needed. Low-potassium periodic paralysis is a rare autosomal dominant hereditary disease. Patients can suddenly develop hypokalemic muscle weakness, and blood potassium is often lower than 3mmol/L. The reason is not fully understood. Acetazolamide can effectively improve muscle weakness. Some patients with hyperthyroidism may also have clinical manifestations of periodic paralysis. The blood potassium may also be temporarily reduced, but the cause may not be exactly the same. Acetazole Amines are not effective, and beta-blockers can significantly improve muscle weakness.

In addition, potassium deficiency, or due to acute, chronic diarrhea caused by intestinal potassium loss is also the main cause of non-nephrogenic hypokalemia.

2. The increase of urinary potassium excretion caused by various causes of renal hypokalemia is the most important cause of hypokalemia. It is collectively referred to as renal hypokalemia. Patients are often accompanied by hypokalemia. Metabolic acidosis or metabolic alkalosis, blood pressure is mostly normal in hypokalemia with metabolic acidosis, and hypokalemia patients with metabolic alkalosis may have hypertension.

(1) hypokalemia accompanied by acidosis: since hypokalemia can compensate for the concentration of plasma sodium bicarbonate, most patients have a tendency to cause alkalosis; conversely, if hypokalemia patients are accompanied by metabolic acid Poisoning is of great help to diagnosis because hypokalemia with acidosis is only seen in renal tubular acidosis, including proximal convoluted tubules and distal convolutic acidosis; and diabetic ketoacidosis.

Diabetic ketoacidosis due to hyperosmolar osmotic diuretic effect and a large number of negatively charged ketone bodies from the urine to promote the discharge of urinary potassium, accompanied by a significant reduction in the body's total potassium, but in acidosis In the early stage, due to the redistribution of intracellular and extracellular potassium, hypokalemia may not be obvious. If potassium is not treated with insulin and alkaline drugs, it may cause severe or even fatal hypokalemia.

(2) hypokalemia and normal blood pH or metabolic alkalosis:

1 primary aldosteronism, serum aldosterone levels increased, and the sodium ions entering the distal convoluted tubules increased significantly, due to increased sodium and potassium exchange urinary potassium excretion, patients with increased levels of blood aldosterone, hypokalemia, but also There are clinical manifestations of hypertension and metabolic alkalosis, and plasma renin activity is mostly decreased. Because hypokalemia can feedback inhibition of adrenal cortex secretion of aldosterone, serum aldosterone levels in patients with severe hypokalemia do not increase correspondingly, normal people or Other causes of hypertensive patients with normal saline or hydrocortisone serum aldosterone should be 110.96nmol / L (4ng / dl), while serum aldosterone levels are not inhibited to help the diagnosis of the disease, adrenal tumors Due to the high level of blood aldosterone, the performance of hypokalemia is also obvious. It must be treated surgically. Adrenal hyperplasia can be tested with spironolactone (Antisophthora) for anti-aldosterone treatment. Most patients with hypokalemia and hypertension can be corrected. The concentration of 18-hydroxyl and 18-oxycortisone in the urine of patients with hyperaldosteronism is increased, and the dexamethasone suppression test is positive, which is a rare Autosomal dominant genetic disease, these patients taking thiazide diuretics can cause very serious hypokalemia while taking low-dose dexamethasone (0.75mg) is able to effectively correct the hypokalemia and decrease blood aldosterone.

2 secondary aldosteronism: the disease is often associated with renal vascular disease, such as renal artery stenosis, renal vasculitis, etc., clinically can also be manifested as hypokale alkalosis and high blood pressure, but it should be noted that not All secondary aldosteronism has hypokalemia, and renal vascular epithelial cells (Robertson-Kihara syndrome) are a rare glomerular para-balloon device that causes an increase in aldosterone due to its secreted renin. Clinically, it also showed hypokalemia and hypertension, and the activity of renal vein renin was significantly increased in the affected side. Some extrarenal malignant tumors may also have an increase in aldosterone, but the serum mainly increased inactive renin levels. .

3 congenital mineralocorticoid syndrome: due to the low activity of congenital 11-hydroxysterol dehydrogenase (11-OHSD), which causes the conversion of cortisol in the kidney to inactive hydroxycortisol, resulting in a large amount of cortisol The mineralocorticoid receptor binds and activates it, exerts a mineralocorticoid-like effect, and clinically shows an increase in aldosterone. Drugs such as licorice, cottonseed phenol and sodium carbenoxate also inhibit 11-OHSD, causing salt cortex. The clinical manifestations of hormonal increase have been reported in the literature due to the intake of food or drugs containing licorice.

4Liddle syndrome: a familial disease, clinically mainly characterized by hypokalemia, hypertension and alkalosis. The pathophysiological characteristics of the intrinsic are characterized by a significant increase in the reabsorption of distal renal tubule sodium, resulting in further expansion of capacity expansion. The production of renin and aldosterone, so the blood aldosterone level of the disease is reduced, sodium retention is the cause of high blood pressure, while increased sodium reabsorption causes increased potassium excretion caused by hypokalemia and alkalosis, patients with erythrocyte membrane sodium ion dysfunction One of the characteristics of this disease, potassium-rich diuretics such as triamterene and amiloride (Amiloride) can be used for the treatment of this disease, on the contrary, spironolactone (anti-Shutong) is not effective for this disease, should not be applied.

5 Cushing's syndrome: about 30% of Cushing's syndrome patients may have hypokalemia, especially in patients with Cushing's syndrome secondary to ectopic corticosteroid secretion, the incidence of hypokalemia is higher, due to sugar Corticosteroids can also produce mineralocorticoid-like effects when combined with mineralocorticoid receptors. Recently, it has been found in animal experiments that glucocorticoids can increase glomerular filtration rate and thus flow through the renal tubules. Increased fluid volume is the main cause of increased urinary potassium excretion.

6 hypochlorine syndrome: hypochloremia is also one of the causes of hypokalemia and metabolic alkalosis, patients without hypertension, hypochloremia often occurs in frequent vomiting or massive loss of chloride ions due to gastrointestinal decompression In addition, long-term use of large doses of thiazide or loop diuretics is also an important cause of hypochloremia.

7Bartter syndrome: Intrinsic is a rare hereditary disease, 80% of patients are under 15 years old, most patients are accompanied by growth retardation, and those over 50 years old are extremely rare. The pathological feature of this disease is the ball side. Hyperplasia of the device, patients may have high renin, hyperaldosteronism, so hypokalemia is also a clinically prominent symptom, due to the prostaglandin, the production of kinins is also significantly increased, so that patients with angiotensin II, armor The action of adrenaline produces resistance, so the patient has no hypertension. Some studies have found that the hypokalemia of this disease is not completely caused by the increase of aldosterone. Because of the restriction of sodium salt intake, taking spironolactone (Antisophthora), ammonia Mitt or excision of the adrenal gland can often effectively reduce urinary potassium excretion in patients with aldosteronism, but these methods can not correct the hypokalemia of Bartter syndrome, on the contrary, prostaglandin inhibitors such as indomethacin (indomethacin) and other drugs But it can correct all the metabolic disorders and abnormalities of this disease, suggesting that prostaglandin production may be the main cause of this disease, in addition to the treatment of this disease should be a prostaglandin inhibitor In addition, potassium should be supplemented in time. For those who have more urinary potassium excretion, potassium-sparing diuretics should be given. Among them, Amiloride is most effective.

8 Magnesium deficiency: Magnesium deficiency can also cause hypokalemia caused by increased urinary potassium excretion. The reason is not clear. Some patients can reduce urinary potassium excretion after supplementing with sufficient magnesium. The clinical manifestations of hypomagnesemia are similar to hypocalcemia. Mainly manifested as muscle tremor, irritability, photophobia, psychosis and other symptoms of increased neuromuscular stress, severe convulsions, convulsions, etc.

9 diuretics: thiazides, acetazolamide, mercury diuretics, and diuretics such as furosemide and etanic acid can cause increased potassium excretion leading to hypokalemia, mainly because these drugs inhibit the kidney Reabsorption of tubule sodium and water, increased sodium and water reaching the distal convoluted tubules, increased Na-K exchange and increased urinary potassium excretion, in addition to these diuretics (except acetazolamide) can also cause metabolic alkalosis, further Increase the excretion of urinary potassium.

In addition to diuretics, there are many other drugs that cause hypokalemia, and the mechanism that causes hypokalemia is not exactly the same. The following table lists some commonly used drugs that cause hypokalemia and the principle of hypokalemia.

(two) pathogenesis

The understanding of the possible pathogenesis of hypokalemia nephropathy comes from the study of experimental hypokalemia in rats. The main cause of renal damage in this disease may be abnormal ammonia production during hypokalemia. The experimental results show that hypokalemia Stimulation of ammonia production, the mechanism of which is intracellular acidosis during hypokalemia, which results in activation of the complement bypass pathway, followed by infiltration of immune cells into the interstitial, resulting in progressive tubulointerstitial damage in hypokalemia Rats were supplemented with sodium bicarbonate to inhibit ammonia production, resulting in a reduction in tubulointerstitial lesions.

The structural and functional changes of tubules associated with potassium loss show reversibility. These lesions do not necessarily develop chronic tubulointerstitial nephropathy and lead to persistent renal insufficiency, but are associated with the duration of hypokalemia. Low potassium has been reported. A familial type of tubulointerstitial nephropathy that exhibits progressive renal failure and experimental hypokalemia in rats. Hyperkalemia can occur for several months after irreversible interstitial fibrosis, but large Rat hypokalemic tubulointerstitial lesions are more serious than humans, and these lesions may be caused by susceptibility to chronic pyelonephritis in hypokalemia rats.

Hypokalemia nephropathy prevention

Prevention: Actively diagnose and treat the primary disease, eliminate various causes of hypokalemia, and strive to correct hypokalemia to prevent the disease from developing and aggravating. Actively diagnose and treat the primary disease, eliminate various causes of hypokalemia, and strive to correct hypokalemia to prevent the disease from developing and aggravating.

Hypokalemia nephropathy complications Complications, pyelonephritis

The disease is easy to be complicated by pyelonephritis and systemic manifestations of hypokalemia. In severe cases, chronic renal insufficiency gradually occurs as the disease progresses.

Hypokalemia nephropathy symptoms Common symptoms Excessive potassium excretion Renal urinary muscle muscle weakness Proteinuria Metabolic acidosis Arrhythmia Polyuria Metabolic hypokalemia Isotonic urine

The manifestations of hypokalemia nephropathy are mainly tubule dysfunction, mainly due to decreased dysfunction, manifested as polydipsia, polydipsia, nocturia, and even renal diabetes insipidus, poor response to vasopressin. There is a small amount of proteinuria and cast in the urine. Early potassium loss can cause metabolic alkalosis. After renal interstitial damage, metabolic acidosis occurs due to renal tubular acidification dysfunction. This disease is complicated by pyelonephritis and urine. The clinical manifestations of road infections gradually appear chronic renal insufficiency as the disease progresses.

In addition to the symptoms of nephropathy, the patient's systemic manifestations mainly include hypokalemia symptoms, such as muscle weakness in the limbs, soft paralysis of the intestines, weakened tendon reflexes, and arrhythmia.

Examination of hypokalemia nephropathy

1. Urine protein and cast type can be seen in urine examination, and more white blood cells are seen in the concurrent infection. The urine concentration dilution test shows that the concentration function is reduced, the urine specific gravity is lowered (the phenol red and the aminopurine acid excretion rate are decreased), and the urinary prostaglandin E is increased. .

2. Blood examination The early blood BUN and Scr can be normal; when renal failure occurs with disease progression, serum creatinine and urea nitrogen levels increase, the characteristic change is blood potassium reduction, and renin and aldosterone increase.

The pathological changes of this disease are tubulointerstitial nephritis, accompanied by progressive renal failure, vacuole formation in proximal convoluted tubules is a pathological feature of hereditary or acquired hypokalemia nephropathy, that is, most vacuoles in renal tubular epithelial cells, especially Proximal tubular lesions are prominent, vacuoles do not contain fat or glycogen, glomeruli and renal blood vessels are generally not damaged, long-term hypokalemia causes tubulointerstitial fibrosis, scar formation, kidney atrophy, pathophysiological changes Renal dysfunction, accompanied by potassium loss, is characterized by vasopressin-resistant urinary concentrating dysfunction, increased ammonia production, decreased glomerular filtration rate, and characteristic structural changes accompanying potassium loss in the human body to the appearance of tubular epithelium The vacuole is due to the expansion of the cell endoplasmic reticulum. This damage is mainly limited to the proximal tubule. The distal tubule has only a focal change. The renal biopsy and imaging examination are routinely performed, and the above characteristic changes can be seen.

Diagnosis and diagnosis of hypokalemia nephropathy

If the clinical cause of significant potassium loss, and the typical clinical and laboratory performance of renal tubular involvement, the diagnosis of this disease can be considered.

Pay attention to the differentiation of chronic interstitial nephritis caused by other causes, such as chronic pyelonephritis, hypercalcemia and nephritis.

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