Some researchers advise that internal intussusception be managed conservatively, compared to external rectal prolapse which usually requires surgery.As with external rectal prolapse, there are a great many different surgical interventions described. Generally, a section of rectal wall can be resected (removed), or the rectum can be fixed (rectopexy) to its original position against the sacral vertebrae, or a combination of both methods. Surgery for internal rectal prolapse can be via the abdominal approach or the transanal approach.It is clear that there is a wide spectrum of symptom severity, meaning that some patients may benefit from surgery and others may not. Many procedures receive conflicting reports of success, leading to a lack of any consensus about the best way to manage this problem. Relapse of the intussusception after treatment is a problem. Two of the most commonly employed procedures are discussed below. laparoscopic ventral (mesh) rectopexy (LVR)
This procedure aims to "[correct] the descent of the posterior and middle pelvic compartments combined with reinforcement of the rectovaginal septum".Rectopexy has been shown to improve anal incontinence (fecal leakage) in patients with rectal intussusception. The operation has been shown to have low recurrence rate (around 5%). It also improves obstructed defecation symptoms.Complications include constipation, which is reduced if the technique does not use posterior rectal mobilization (freeing the rectum from its attached back surface).The advantage of the laparoscopic approach is decreased healing time and less complications.
Treatments for anemia and bone disease may also be required. Severe disease requires hemodialysis, peritoneal dialysis, or a kidney transplant for survival.Chronic kidney disease affected 753 million people globally in 2016 - 417 million females and 336 million males. In 2015, it caused 1.2 million deaths, up from 409,000 in 1990. The causes that contribute to the greatest number of deaths are high blood pressure at 550,000, followed by diabetes at 418,000, and glomerulonephritis at 238,000. Signs and symptoms
CKD is initially without symptoms, and is usually detected on routine screening blood work by either an increase in serum creatinine, or protein in the urine. As the kidney function decreases, more unpleasant symptoms may emerge:
Blood pressure is increased due to fluid overload and production of vasoactive hormones created by the kidney via the renin–angiotensin system, increasing the risk of developing hypertension and heart failure. People with CKD are more likely than the general population to develop atherosclerosis with consequent cardiovascular disease, an effect that may be at least partly mediated by uremic toxins. People with both CKD and cardiovascular disease have significantly worse prognoses than those with only  cardiovascular disease. Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Due to its high systemic concentration, urea is excreted in eccrine sweat at high concentrations and crystallizes on skin as the sweat evaporates ("uremic frost"). Potassium accumulates in the blood (hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias).