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Type IV renal tubular acidosis

  Type IV renal tubular acidosis (type IV renal tubular acidosis), also known as hyperkalemia renal tubular acidosis. It is caused by insufficient aldosterone or antagonism. Its clinical features are hyperkalemia, hyperchlorhydric acidosis, reduced excretion of urine ammonia, salt loss in the kidney, and moderate decline in glomerular filtration function.

Table of Contents

What are the causes of type IV renal tubular acidosis?
What complications can type IV renal tubular acidosis easily lead to?
3. What are the typical symptoms of type IV renal tubular acidosis
4. How to prevent type IV renal tubular acidosis
5. What laboratory tests need to be done for type IV renal tubular acidosis
6. Dietary taboos for patients with type IV renal tubular acidosis
7. Conventional methods for the treatment of type IV renal tubular acidosis in Western medicine

1. What are the causes of the etiology of type IV renal tubular acidosis?

  One, Etiology

  The main causes of type IV RTA are due to three factors: aldosterone deficiency, tolerance to the action of aldosterone in the collecting tubules, and voltage dependence. Many diseases can cause type IV RTA.

  1, Aldosterone deficiency

  Diseases that cause hypoaldosteronism with low reninemia, such as various chronic tubulointerstitial kidney diseases, diabetic nephropathy, hypertensive renal sclerosis, or renal transplantation, can all cause aldosterone deficiency and secondary insufficient renin secretion. Addison's disease and congenital defects in aldosterone synthesis can also lead to insufficient aldosterone secretion.

  2, Decreased responsiveness of the kidney to aldosterone

  Diseases associated with secondary hyperreninemia and hyperaldosteronemia, such as pseudoaldosteronism, salt-losing nephritis, and various tubulointerstitial lesions (abuse of analgesics, sickle cell disease, and obstructive nephropathy), and others.

  4, Voltage-dependent

  It is mainly seen after the use of triamterene, sickle cell anemia, and other diseases.

  Two, Pathogenesis

  Under normal circumstances, the cortical collecting tubules of the distal renal units increase the absorption of Na under the regulation of aldosterone, promoting the secretion of K and H. The pathogenesis of this type of renal tubular acidosis is not yet fully understood. It is currently believed that aldosterone deficiency and reduced responsiveness of the distal renal tubules to aldosterone are the main pathogenic factors. Aldosterone deficiency prevents the distal renal tubules from retaining Na, excreting K, excreting Cl-, and secreting H, leading to hyperchloremic acidosis and hyperkalemia. Renin deficiency is the main cause of hypoaldosteronism, followed by insufficient angiotensin II, disturbances in the biosynthesis of the glomerular cortex of the adrenal cortex, and others. Insufficient renin secretion is related to the structural and functional abnormalities of the juxtaglomerular apparatus. Glomerulosclerosis and interstitial fibrosis can both lead to damage to the juxtaglomerular apparatus. Other factors such as defects in the conversion of renin precursors, lack of prostacyclin, volume expansion, and the effect of endothelin are also related to reduced renin secretion. The low responsiveness of the renal tubules to aldosterone may be related to damage to the aldosterone receptors in the renal tubules, mainly type II receptors. Studies have shown that hypoaldosteronism is not related to renal function damage. However, a decrease in endogenous creatinine clearance is positively correlated with the excretion of NH3 in urine. This suggests that certain mild renal function damage in DRTA may be related to structural and functional damage in the distal renal tubules. The lesion not only involves the functional defect of the alpha intercalating cell H pump but also affects the principal cells, causing defects in Na-K transport, hence also known as total distal renal tubular acidosis. In addition, some propose that this type of renal tubular acidosis is due to excessive reabsorption of chlorine (chloride shunt theory). Since the reabsorption of chlorine is relatively more than sodium, the increase in NaCl in the body leads to expansion of the extracellular fluid, increased blood pressure, and decreased blood renin and aldosterone; at the same time, the transmembrane potential of the distal renal tubules decreases, causing potassium secretion disorders, leading to hyperkalemia and acidosis. In addition, the pathogenesis varies due to different underlying diseases:

  1. Chronic tubular and interstitial kidney disease caused by

  The function of distal renal tubule cells is damaged, the excretion of H and K is reduced, the production of ammonia is reduced, leading to the reduction of ammonia excretion, and the occurrence of acidosis and hyperkalemia, or due to the simultaneous obstruction of HCO-3 reabsorption by the proximal renal tubules, a large amount of HCO-3 is lost in the urine, and the acidosis is aggravated.

  2. Insufficient aldosterone secretion or reduced aldosterone response of the renal tubules

  The cause is the obstruction of H and K excretion in the distal renal tubules, leading to the retention of H and K in the body, the loss of HCO-3 from the urine, and the occurrence of acidosis and hyperkalemia. Hyperkalemia inhibits the production of ammonia by the kidneys (the most important urinary buffering substance), thereby limiting the excretion of H and aggravating acidosis.

2. What complications can type IV renal tubular acidosis easily lead to

  Type IV renal tubular acidosis may complicate with hyperchloremic acidosis, mild to severe renal insufficiency. In the late stage, it may be accompanied by hypertension and cardiac insufficiency, seriously affecting the health of patients, so timely treatment is required.

3. What are the typical symptoms of type IV renal tubular acidosis

  This type is more common in the elderly, and most patients have some type of kidney disease, such as diabetic nephropathy, hypertensive nephropathy, and chronic tubulointerstitial disease. 70% have mild to severe renal insufficiency. The type of kidney disease is most common in diabetic glomerulosclerosis, followed by tubulointerstitial nephritis.

  The clinical manifestations are hyperchloremic acidosis and persistent hyperkalemia. Generally speaking, when the GFR is greater than 10-15ml/min before the terminal stage of chronic renal failure with oliguria, it is rare to have potassium excretion disorders. However, in this type of patients, when the GFR is greater than 20ml/min, there is obvious hyperkalemia and acidosis. Most patients have hypoaldosteronism with low reninemia, and the concentration of plasma renin and aldosterone is reduced, even when the extracellular volume is insufficient. This is not proportional to the degree of renal dysfunction, so it is not related to glomerular lesions. It is mainly due to tubular dysfunction. Hyperkalemia can be asymptomatic, or can manifest as muscle weakness, arrhythmia, abnormal electrocardiogram, and in a few patients, even heart block and hyperkalemic paralysis.

  For those with metabolic acidosis accompanied by persistent hyperkalemia, and cannot be explained by glomerular dysfunction or other causes, the possibility of this disease should be considered. If there are etiologies of the primary disease (such as primary adrenal cortical hormone deficiency or deficiency, chronic tubulointerstitial nephritis, drug toxicity, etc.), an increase in urinary HCO3- excretion, a decrease in urinary ammonium, a decrease in plasma renin, and aldosterone content are helpful for diagnosis. The GFR of this disease often has a slight decrease (≥30ml/min), while the GFR of glomerular dysfunctional RTA is usually

4. How to prevent type IV renal tubular acidosis

  1. Patients with severe renal tubular acidosis need to rest in bed. And be given a light diet with high calories, high protein, and a variety of vitamins;

  1. The patient with severe renal tubular acidosis needs to rest in bed. And be given a light diet with high calories, high protein, and a variety of vitamins;

  2. It is also necessary to accurately record the intake and output, and do all kinds of laboratory tests. The intake and output are important indicators reflecting the water, electrolyte, and acid-base balance in the body, which can directly reflect the changes in the patient's condition, and various laboratory tests also provide good evidence for the diagnosis of the disease, so it is necessary to correctly collect various specimens such as blood and urine and send them for timely testing.

5. What laboratory tests are needed for type IV renal tubular acidosis

  1. Blood test

  Increased blood potassium, increased blood chloride, decreased blood bicarbonate, decreased CO2 binding power, most patients have moderate elevation of blood urea nitrogen and creatinine, the activity of plasma renin and aldosterone varies with the primary disease, most of which are reduced due to kidney disease; a few infant patients (reduced aldosterone response in renal tubules) have normal or increased plasma renin and aldosterone, and type IV RTA caused by adrenal cortical disease has reduced plasma aldosterone and often increased plasma renin activity.

  2. Urinalysis

  Type IV RTA shows acidic urine (urine pH

6. Dietary taboos for patients with type IV renal tubular acidosis

  Patients with type IV renal tubular acidosis should eat alkaline foods, potassium-rich foods (watermelon, oranges), and foods containing vitamin D (cod liver oil), and the dietary structure should be reasonable and nutrition-rich.

7. Conventional methods for treating type IV renal tubular acidosis in Western medicine

  This disease is not rare and we should be vigilant to avoid misdiagnosis. Pay attention to the characteristics such as hyperchloremia, hypokalemia or hyperkalemia, atypical alkaline urine, polydipsia, polyuria, and delayed growth and development, and further expand the examination to achieve early diagnosis and timely and reasonable treatment to reduce complications and damage to kidney function. At the same time, look for secondary causes of disease and actively treat the primary disease. Alkaline drugs should be selected according to different types and conditions, and long-term to lifelong medication should be taken. On the other hand, regular outpatient follow-up for patients is of great importance for guiding treatment, adjusting drugs, and protecting kidney function and reducing complications.

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