Type IV renal tubular acidosis

Introduction to type IV renal tubular acidosis Type IV renal tubular acidosis (type IVrenal tubular acidosis), also known as hyperkalemia type renal tubular acidosis. It is caused by insufficient or antagonistic aldosterone. Its clinical features are hyperkalemia, high blood chlorine acidosis, reduced urinary ammonium excretion, renal loss of salt and moderate glomerular filtration. basic knowledge Sickness ratio: 0.05% Susceptible people: no special people Mode of infection: non-infectious Complications: high blood pressure

The cause of type IV renal tubular acidosis

(1) Causes of the disease

The main cause is aldosterone deficiency, the resistance of the collecting tube to aldosterone and voltage dependence, and many diseases can cause type IV RTA.

1. Aldosterone deficiency causes diseases of hyporeninitis with low aldosteronism, such as various chronic tubules, interstitial kidney disease, diabetic nephropathy, hypertensive nephrosclerosis or kidney transplantation, etc., can cause aldosterone deficiency and secondary kidney Insufficient secretion, and Addison disease, defects in congenital aldosterone synthesis can also lead to insufficient aldosterone secretion.

2. The kidney has reduced reactivity to aldosterone, accompanied by secondary hyperreninemia and hyperaldosteronism, such as pseudo aldosterone deficiency, salt-salt nephritis and various tubulointerstitial lesions (abuse of painkillers, Sickle cell disease and obstructive kidney disease).

3. Voltage dependence is mainly seen after the use of triamterene, sickle cell anemia and the like.

(two) pathogenesis

Under normal circumstances, the cortical collecting duct of the distal nephron is under the regulation of aldosterone, which increases the absorption of Na and promotes the secretion of K and H. The pathogenesis of this type of renal tubular acidosis is not fully understood. It is currently considered that aldosterone deficiency and distal kidney The reduction of aldosterone response in tubules is the main pathogenesis. The lack of aldosterone prevents the distal tubules from retaining Na, draining K, discharging Cl-, secreting H and causing hyperchloric acidosis and hyperkalemia. Renin deficiency is hypoaldosteronism. The main causes include angiotensin II deficiency, adrenal cortical globular band biosynthesis or disorder, and insufficient renin secretion is associated with structural and dysfunction of the juxtaglomerular apparatus, glomerular sclerosis and interstitial fibrosis. Can cause damage to the juxtaglomerular apparatus, other, prorenin precursor transformation disorders, prostacyclin deficiency, volume expansion, endothelin action is also associated with decreased renin secretion, renal tubular response to aldosterone may be associated with renal tubules Aldosterone receptor damage, mainly type II receptors, studies have shown that low aldosteronism is not associated with renal dysfunction, while endogenous creatinine clearance decreases with urine NH 3 positive correlation, suggesting that some mild renal damage DRTA may be related to distal renal tubular structure and functional damage, the lesion not only involves the interstitial H cell pump function defects, but also the main cell caused by Na-K malfunction, It is also known as total distal renal tubular acidosis. In addition, it has been suggested that this type of renal tubular acidosis is due to excessive reabsorption of chlorine (chlorine shunt theory), because the reabsorption of chlorine is relatively more than sodium, so the body Increased NaCl, extracellular fluid expansion, elevated blood pressure and decreased blood renin and aldosterone; at the same time, the distal renal tubular transmucosal potential decreased, thus the secretion of potassium, causing hyperkalemia and acidosis, in addition, its pathogenesis The disease varies and is different:

1. Chronic tubules, interstitial kidney disease caused by distal renal tubular cell function damage, decreased H, K, decreased ammonia production caused by decreased ammonia, acidosis and hyperkalemia, or because of proximal Renal tubules are re-absorbed by HCO-3, and a large amount of HCO-3 is lost in the urine, which is aggravated by acidosis.

2. Insufficient aldosterone secretion or reduced renal tubular response to aldosterone, distal renal tubules excrete H and K disorders, so that H and K are retained in the body, HCO-3 is lost from the urine, and acidosis and high potassium occur. Hypertension, hyperkalemia, is caused by inhibition of renal ammonia production (the most important urinary buffer), which limits H discharge and increases acidosis.

Type IV renal tubular acidosis prevention

This disease is not uncommon, we must be vigilant to avoid missed diagnosis, catch hyperchloric acidemia, hypokalemia or hyperkalemia, abnormal alkaline urine, polydipsia, polyuria, growth retardation and other characteristics, further check and strive for Early diagnosis and timely and reasonable treatment to reduce the complication of comorbidities and renal function, while looking for the following causes, actively treating the primary disease, should choose basic drugs according to different types and conditions, and take drugs for a long time and even life, on the other hand, Regular follow-up visits by patients to guide treatment, adjust drugs, and play an important role in protecting kidney function and reducing complications.

Complications of type IV renal tubular acidosis Complications

High blood chlorine acidosis, mild to severe renal insufficiency, advanced hypertension, and cardiac insufficiency.

Type IV renal tubular acidosis symptoms Common symptoms Nausea and vomiting Nausea bone pain Lack of kidney calcification Polyuria dehydration Hypertension

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

The clinical manifestations are high blood chlorine acidosis and persistent hyperkalemia. Generally speaking, when chronic renal failure does not reach the end stage oliguria stage GFR>10~15ml/min, there is little potassium excretion disorder, and this type Patients with GFR>20ml/min had significant hyperkalemia and acidosis, most of them had low renin-induced hypoaldosteronism, and plasma renin and aldosterone concentrations were reduced, even when extracellular capacity was insufficient. This is not proportional to the degree of renal insufficiency, so it has no major relationship with glomerular lesions, but mainly due to renal tubular dysfunction, hyperkalemia can be asymptomatic, can also be expressed as muscle weakness, arrhythmia, abnormal ECG Etc., a small number of patients may even have heart block and high potassium paralysis.

Anyone with metabolic acidosis associated with persistent hyperkalemia who cannot be explained by glomerular insufficiency or other reasons should consider the possibility of the disease, such as the primary onset of the disease (eg primary adrenal gland) Insufficient or lack of corticosteroids, chronic tubulointerstitial nephropathy, drug toxicity, etc.) Increased urinary HCO3-discharge, decreased urinary ammonium, decreased plasma renin, and decreased aldosterone levels, which is often helpful in the diagnosis of GER. 30ml / min), and glomerular insufficiency RTA, its GFR is often <30ml / min.

Examination of type IV renal tubular acidosis

1. Blood examination increased blood K, blood Cl- increased, blood HCO-3 decreased, CO2 binding decreased, blood urea nitrogen and creatinine were moderately elevated in most patients, plasma renin and aldosterone activity varied according to the primary disease. Plasma renin and aldosterone levels are mostly reduced in patients with kidney disease; a small number of infant patients (kidney tube weakened to aldosterone) normal or elevated plasma renin and aldosterone, type IV RTA caused by adrenal cortical disease, plasma aldosterone reduction Plasma renin activity tends to increase.

2. Urine examination Type IV RTA is acidic when urine acidosis (urinary pH<5.5) is free of HCO3-, and the filtered HCO3-reabsorption is reduced when oral alkaline drug keeps plasma HCO3- normal ( <15%), HCO3- appears in the urine, but usually only accounts for 2% to 3% of the total filtration, not more than 10%, the urine NH4 excretion is significantly reduced, but no diabetes, amino acid urine or urinary phosphate excretion increases, Glomerular filtration rate (GFR) was measured normally.

Routine imaging examination, X-ray examination, B-ultrasound and electrocardiogram examination.

Diagnosis and diagnosis of type IV renal tubular acidosis

Diagnostic criteria

The main points of diagnosis of type IV RTA are:

1. Clinically diagnosed renal tubular acidosis.

2. There is chronic kidney disease or adrenal cortical disease.

3. Sustained hyperkalemia with decreased plasma aldosterone activity, suspected of the disease.

According to the different pathogenesis of type IV RTA, some people divide it into several subtypes.

Differential diagnosis

Type IV RTA should be differentiated from type I RTA with hyperkalemia. Type II RTA is mainly due to low pH gradient. According to its low potassium level, HCO3-reabsorption is normal, urine pH>6.0, urine NH4. The characteristics of significantly reduced excretion are not difficult to identify.

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