Proximal (type II) renal tubular acidosis

　　The etiology of proximal (Type II) tubular acidosis includes two types: primary and secondary. The specific etiology and mechanism are as follows:

　　Section 1: Primary The cause is unknown, and it is generally believed to be related to heredity. It only manifests as HCO3- reabsorption disorder without other renal tubular and glomerular dysfunction. Sporadic, in infants it is temporary; hereditary, it is persistent, showing autosomal dominant inheritance or autosomal recessive inheritance.

　　Section 2: Secondary It often occurs secondary to systemic diseases, which can be accompanied by various renal tubular dysfunction, with Fanconi syndrome being the most common.
　　1. Accompanied by other genetic diseases: genetic diseases accompanied by other proximal renal tubular dysfunction, such as idiopathic Fanconi syndrome, cystinosis, eye-brain-kidney syndrome (Lowe syndrome), hereditary fructose intolerance, tyrosinemia, galactosemia, glycogen storage disease, etc.
　　2. Drug and toxin-induced kidney damage: such as carbonic anhydrase inhibitors, methyl 3-cyanate, malonate intoxication, heavy metal (calcium, lead, copper, mercury) intoxication, etc.
　　3. Other: such as subacute necrotizing myelopathy (Leigh syndrome), tetralogy of Fallot, malabsorption of the intestines, hyperparathyroidism, hereditary nephritis, chronic rejection after kidney transplantation, multiple myeloma, amyloidosis, chronic active hepatitis, medullary cystic disease of the kidney, Wilson's disease, etc.

　　Proximal renal tubular acidosis (PRTA) is also known as Type II PRTA. The primary PRTA mostly occurs in children, most of which start from childhood and may be related to heredity; secondary PRTA is often caused by systemic diseases, drug intoxication, and Fanconi syndrome, etc. Proximal (Type II) tubular acidosis can have complications such as osteomalacia, growth and development delay, etc.

　　The symptoms of proximal (Type II) tubular acidosis are usually mild, manifested as malnutrition, easy fatigue, anorexia, polyuria, polydipsia, or hypokalemia. Typical cases have hyperchlorhydria, but the distal tubular acidification function is normal, and the urine pH can drop below 5.5, or accompanied by bone damage (osteomalacia, osteoporosis), diabetes, aminoaciduria, and other conditions.

　　Proximal (Type II) tubular acidosis of primary origin, due to the unknown cause, has no reliable preventive methods. Clinically, it mainly focuses on the secondary cases caused by drug and toxin-induced kidney damage and other diseases such as malabsorption of the intestines, hyperthyroidism, and active prevention to prevent the prolonged metabolic acidosis, causing systemic metabolic disorder and kidney function damage.

　　The diagnosis of proximal (Type II) tubular acidosis, in addition to clinical manifestations, also requires auxiliary examination, which is an indispensable means. The following are common examinations:
　　Section 1: Blood Biochemical Examination
　　1. Blood pH value, HC03— or cch binding capacity decreased;
　　2. Blood chloride significantly elevated, blood potassium significantly decreased, and anion gap can be normal.
　　Section 2: Urinalysis
　　1. Urine specific gravity and osmotic pressure decrease;
　　2. Urine pH > 6. When acidosis worsens, blood HCO3—　　Third, other auxiliary examinations
　　Routine electrocardiogram, imaging examination and B-ultrasound examination.

　　Patients with proximal (type II) renal tubular acidosis should eat high-calorie, low-protein foods; eat foods rich in dietary fiber; eat foods with diuretic effects. Patients should avoid eating foods high in salt; avoid eating high-potassium foods; avoid eating foods high in protein content.

　　The clinical manifestations of proximal (type II) renal tubular acidosis are similar to those described in the TCM section of 'Kidney Labor' in the TCM department of injury. The disease originates internally and is mainly related to internal injury factors. It may be due to insufficient endowment from birth, or due to seven emotions, diet, and fatigue, which injure kidney essence and become symptoms of deficiency and injury. The specific TCM differential diagnosis and treatment methods are as follows:

　　1. Deficiency of Kidney Essence
　　Treatment Method: Tonify the kidney and fill essence.
　　Prescription: Can use Baitian Dazao Pill, Liushen Wanyin Pill, Zuogui Pill or Zuogui Drink with modifications. Medicines include Shudihuang, Shanyao, Shanyao, Gouqizi, Guizhu, Lujiaojiao, Duzhong, Tusizi, Danggui, Niuxi, Wuweizi, Yuanzhi, etc. The combined use of these herbs can tonify the kidney and fill essence, strengthen the waist and knees, and enhance intelligence and open the orifices.

　　2. Deficiency of Spleen Qi
　　Treatment Method: Regulate Qi and invigorate the spleen.
　　Prescription: Use Xiangsha Liujunzi Decoction with modifications. Medicines include Dangshen, Baizhu, Fuling, Gancao, Chenpi, Banxia, Muxiang, Shaoren, Koushen, Zhipu, Dafupi, Tongcao. The six herbs in the formula regulate Qi and invigorate the spleen, and Koushen, Zhipu, Dafupi, and Tongcao are added to strengthen the power of transforming turbidity and invigorating the spleen. If spleen dampness transforms into heat, treatment with Huanglian Wending Decoction and other modifications can be used.

　　3. Deficiency of Stomach Yin
　　Treatment Method: Nourish stomach Yin.
　　Prescription: Use Yiguan Decoction, Yunuoyan or Shashen Maidong Decoction combined with Shengmai Powder with modifications. Medicines include Taizishen, Maidong, Wuweizi, Shashen, Zhimu, Baihe, Yuzhu, Shudi, Niuxi, Tianhuafen, Banxia, Chenpi, etc. The combined use of these herbs nourishes Yin and generates body fluid, benefits the stomach, and has the effect of nourishing kidney Yin.

　　4. Deficiency of both Yin and Yang
　　Treatment Method: Tonify both Yin and Yang.
　　Prescription: Use Jinkui Shenqi Pill or Dihuang Yinzhi Decoction with modifications. Medicines include Shudihuang, Maidong, Wuweizi, Shanyao, Zhifupian, Rougui, Baizhitai, Rourong, Yuanzhi, Zhipu, Zhiziren, Gouqizi, Tusizi, etc.