Sleep disordered breathing is an emerging fringe discipline, which mainly includes snoring, obstructive sleep apnea hypoventilation syndrome, central sleep apnea hypoventilation syndrome, sleep hypoventilation syndrome, chronic obstructive pulmonary disease and sleep disordered breathing caused by neuromuscular disorders, among which obstructive sleep apnea hypoventilation syndrome is the most common. Sleep breathing disorders are closely related to several disciplines. In the following, we mainly take obstructive sleep apnea hypoventilation syndrome as the representative to explain the relationship between sleep breathing disorders and renal pathology. The incidence of OSAHS combined with proteinuria/nephrotic syndrome: OSAHS combined with proteinuria or even nephrotic syndrome is often reported. the incidence of OSAHS combined with proteinuria varies from 33-64%, depending on the detection method and the definition criteria for proteinuria. The renal pathological changes of OSAHS combined with proteinuria/nephrotic syndrome: OSAHS combined with proteinuria is mostly functional and reversible, which can be reduced or even disappeared with the improvement of OSAHS treatment. renal pathological changes of OSAHS combined with proteinuria mainly show glomerular hypertrophy, microscopic lesions, thylakoid proliferative changes and focal segmental sclerosis. Light microscopy is normal or glomerular volume increases, thylakoid cells proliferate, thylakoid stromal accumulation and focal sclerosis, immunofluorescence is negative, electron microscopy can be normal or have epithelial cell peduncle fusion and basement membrane thickening. 3, pathogenesis of OSAHS combined proteinuria/nephrotic syndrome: For the mechanism of OSAHS combined proteinuria, most scholars believe that the repeated hypoxia and hypercapnia caused by OSAHS can successively cause pulmonary hypertension, elevated right atrial pressure, elevated central venous pressure, elevated renal venous pressure, and elevated glomerular capillary hydrostatic pressure, thus causing the lattice structure of the glomerular basement membrane This results in reversible changes in the lattice structure of the glomerular basement membrane, with the result that proteins are filtered through the basement membrane, producing proteinuria. Recent studies have concluded that obesity and hypertension in OSAHS patients also play a role in the production of proteinuria. OSAHS and renal function changes: OSAHS can lead to nocturnal renal function changes, which are mostly functional and reversible. nocturnal urine volume, urinary sodium and urinary chloride excretion increase significantly in OSAHS patients, and the rate of filtered sodium reabsorption decreases significantly, but these indicators return to normal after CPAP treatment. Krieger et al. determined that the level of ANP in the pulmonary artery of OSAHS patients with sleep apnea was significantly increased; our study showed that The results of decreased proximal tubular sodium reabsorption rate and absolute value and distal tubular sodium reabsorption rate in OSAHS patients are consistent with the renal natriuretic effect of ANP; in addition, our study also showed that the decrease in osmotic pressure in OSAHS patients was accompanied by no change in free water clearance, which is consistent with ANP decreasing the osmotic pressure gradient in the renal cortex-medulla and disrupting the urinary reflux multiplication mechanism The increase in ANP secretion is secondary to the tight closure of the upper airway during sleep apnea, the significant increase in negative intrathoracic pressure during forceful inspiration, the increase in right atrial return blood volume and apnea-induced hypoxia, pulmonary vasoconstriction, and increased right ventricular afterload, both of which lead to right atrial dilatation, which stimulates increased ANP secretion. Sleep respiratory disturbances in end-stage renal disease In chronic renal insufficiency (CRI), the accumulation of protein toxic metabolites in the body causes metabolic, hematopoietic, neurological, and gastrointestinal impairment, which also affects the respiratory system and leads to SDB. SDB is very common in uremia, with up to 80% of long-term dialysis patients complaining of sleep disturbances and daytime sleepiness. Although the vast majority of the general population has obstructive apnea, the incidence of obstructive and central apnea is equal in uremic patients, and uremic patients with comorbid cardiac failure usually exhibit mainly central apnea. 1, pathogenesis The mechanism of combined SDB in patients with CRI is not fully understood. It is generally believed that it is related to the patient’s chronic metabolic acidosis, the accumulation of medium-molecule toxic substances in the body, the increase of upper airway resistance due to pharyngeal edema caused by water retention, dialysis itself, and the level of branched-chain amino acids in the body. (1) Chronic metabolic acidosis: Hypocapnia due to chronic metabolic acidosis in CRI can make the partial pressure of carbon dioxide close to the apnea-causing domain level, and the patient is prone to periodic breathing, followed by apnea. abnormal ventilation during CRI is an adaptive response to chronic metabolic acidosis. It has been demonstrated that the organism can recover a normal ventilatory response to carbon dioxide stimulation after hemodialysis. However, after 24 hours, this response returns to its original level. In addition, chronic metabolic acidosis can increase the sensitivity of the respiratory response to hydrogen ions, causing the patient to have a shortened respiratory response arc and an unstable respiratory pattern, which can lead to apnea. (2) Uremic toxin: Fein et al. observed that SDB could be relieved after hemodialysis in patients with CRI, and therefore proposed that uremic toxin could act on the central nervous system to cause apnea in patients with reduced upper airway muscle tone or unstable respiratory control during sleep. lanjevin B et al. reported 2 patients with end-stage renal failure combined with severe OSAHS who received both maintenance hemodialysis and CPAP therapy. This was further supported by the complete resolution of SDB symptoms and significant improvement in PSG monitoring after successful kidney transplantation. (3) Other factors affecting the opening of the upper airway: The primary disease of CRI patients (such as diabetes) and peripheral neuropathy caused by CRI itself and edema caused by excessive volume loading in CRI patients can affect the opening of the upper airway and lead to apnea. (4) Dialysis: It is thought that dialysis itself is also responsible for the occurrence of apnea, and it is believed that hemodialysis can lead to apnea by causing an imbalance in the patient’s osmotic pressure. Wadhawa compared the incidence of SDB in patients on hemodialysis with those on abdominal dialysis and concluded that abdominal dialysis was more prone to SDB than hemodialysis. (5) Branched-chain amino acid levels in the body: Soreide et al. reported seven cases of uremic patients receiving branched-chain The patients in the branched-chain amino acid group recovered their rapid eye movement sleep time from a lower level to normal, and the end-breath carbon dioxide exhalation in all phases of sleep was significantly reduced, and only one patient developed sleep apnea; while their AHI decreased from 85 to 31, while all central apnea disappeared and blood oxygen saturation improved significantly, suggesting that the low level of branched-chain amino acids in CRI patients can cause apnea, but the exact mechanism is not clear. 2. Diagnosis Although formal diagnosis of sleep apnea requires polysomnography monitoring, nighttime finger oxygen monitoring at home in patients with end-stage renal disease is a good screening tool, and positive results suggest the presence of true sleep apnea. 3. Treatment (1) Etiology: The treatment of patients with RI combined with SDB should first be directed at the etiology. ① Kidney transplantation can completely replace the function of the kidney, and several scholars have reported individual cases of complete remission of SDB after kidney transplantation. (2) Adequate hemodialysis, especially HDF, which is more effective in removing medium and small molecule toxins, peritoneal dialysis, which is more effective in removing medium molecule toxins, and HF can partially improve the symptoms. (2) Treatment of sleep apnea: The treatment for sleep apnea mainly depends on whether the type of apnea is obstructive or central. (1) Obstructive sleep apnea: The treatment for obstructive apnea is mainly the correction of its pathophysiological changes, such as weight loss, avoidance of alcohol and sedative drugs, continuous positive pressure ventilation (CPAP) treatment, oral appliances or surgical treatment, etc. ②Central sleep apnea: Patients with hypoxic central sleep apnea usually respond better to nocturnal oxygen therapy. CPAP is also effective for central sleep apnea, especially when the patient’s central apnea is secondary to congestive heart failure, and CPAP and theophylline are more effective options.