Indications
Longterm bladder catheter encrustation
If a patient has to be treated with an indwelling bladder catheter for more than 4 weeks, he/she qualifies as chronic (longterm) catheter carrier. Based on published studies, about 4% of all human beings living at home carry such a catheter, whereas the prevalence of bladder catheter carriers in nursing homes exceeds 8%.
Urinary tract infection (UTI) is a frequent and the most important complication for patients with bladder catheters. The risk for infection rises 3-7% per day of an indwelling catheter in situ. Up to 30% of catheter carriers experience a urinary tract infection every year. The process starts with biofilm or crystallization formation by urease-producing bacteria and crystals in urine such as oxalate and ends with a blockage of the catheter. Up to 50% of these patients are suffered from encrustation and/or a blockage per year. A blockage requires an immediate emergency replacement of the catheter, otherwise, repeated blockage could damage the kidneys. Another complication is the building of bladder stones. Today there is no pharmacological treatment available to prevent or reduce these complications. Nursing home residents with a urinary catheter are three times more likely to die, be hospitalized, or require antibiotics than those without a catheter. These health risks for people with urinary catheters could be reduced through evidence-based care and support for self-management. One option for these patients are routinely catheter change every 4 to 6 weeks.
Various sterile irrigation solutions are used to reduce/prevent the formation of biofilms and inhibit crystallization processes, which promote catheter obstructions and thus frequent catheter changes, e.g. Uro-Tainer® NaCl 0.9% (single-use system for intravesical instillation and mechanical rinsing of the catheter and bladder); or Uro-Tainer® Suby G (single-use system for intravesical instillation to prevent crust formation). Apart from the material and care requirements, the disadvantage of these solutions is that they are designed for a single use and only remain in the bladder temporarily.
An oral alkali-citrate mixture, which permanently modulates the environment in the bladder in a positive sense, would be highly appreciated and suitable so that indwelling catheters could remain in situ for a longer time. If this drug is available in liquid form, this would be a further advantage, because the fluid amount could simultaneously supply sufficient fluid for diuresis. Finally, catheter wearers would be spared unnecessary catheter changes with possible complications and increased costs.
Prevention of secondary kidney stones
The development of kidney stones (Nephrolithiasis) is a widespread disease associated with painful episodes, hospitalizations, and, not neglectable, surgical interventions. The causes of stone formation are low fluid intake, too few vegetables and fruits (citrates), too much oxalate and animal protein,s and excessive salt intake. All of these boosters should be counteracted so that the mineral concentrations in the urine can be reduced and any crystallization can be prevented. Approximately 80–90% of kidney stones contain calcium in different salt forms. The increased urinary excretion of calcium, oxalate, and low citrate are the most striking features of these patients. Kidney stones occur more frequently in western countries. The recurrence rates after the first episode of stone formation increase strongly from 40% within the first 5 years to 50% within 10 years and over 75% within 20 years. Therefore, it is very important to prevent these relapses because each episode of a stone formation is harmful to the kidneys.
Chronic kidney disease with metabolic acidosis
Disorders of the renal function and/or pathological changes in the renal structure are triggers of a renal failure. The capacity of the kidneys to excrete urophanic metabolic substances decreases. The more advanced the disease symptoms are, the higher the incapability to keep the acid-base balance in the blood. So, a renal failure primarily affects the acidity regulation. That’s the starting point for the development of metabolic acidosis in connection with renal impairment. The bicarbonate buffer system will change towards a deficit. The incidence of metabolic acidosis increases proportionally according to the degree of the renal failure and with the decrease of the renal function, respectively. This kind of acidosis connected with a chronic kidney disease (CKD, stage 2 to 4) must be treated as early as possible and for a long time. This will contribute to the recovery of the renal function and restore homeostasis. The latter must be sought in view of the proven long-term complications of metabolic acidosis: e.g., impairment of the muscle metabolism, decrease of the bone mineral density, decrease of the insulin effectiveness, and reduction of the cardiac function.
Chronic metabolic acidosis
A well-functioning buffer system guarantees that the concentration of acids and bases in the body is well balanced and, therefore, all biological and physiological processes in the body perform at their best. The buffer system is regulated by the kidneys’ filtration and excretion and ensures that the blood pH value ranges between 7.35 and 7.45. The lifestyle is crucial. An unbalanced diet, e.g. excessive consumption of animal proteins and various genetic or acquired diseases can adversely disrupt this buffering system and thus facilitate metabolic acidosis. However, this does not produce any immediate symptoms. But if this condition remains unchanged over a longer period of time, various complications or secondary organic lesions can occur. One of the long-term symptoms is the loss of bone substance, that will result finally in an osteopenia and osteoporosis. This also amplify the age-related decrease of the kidney function. The effectiveness of insulin will be reduced, which can promote the beginning of a diabetes mellitus. A further possible complication is be the formation of kidney stones.
Disturbed glucose tolerance
The measurement of the blood sugar concentration serves as a simple parameter for the diagnosis and differentiation of the various disorders of the blood sugar level up to diabetes mellitus. The disturbed glucose tolerance is evident from a slightly pathological fasting glycemia. However, the oral glucose tolerance test shows abnormal values. Impaired glucose tolerance is likely to be widespread in the Western population. In particular, patients with a metabolic syndrome from a complex of abdominal obesity, hypertriglyceridemia, arterial hypertension, and an impaired carbohydrate metabolism are exposed to this risk. Dysfunctional glucose tolerance is quite manifold in terms of negative effects. Well-known are for example, changes in insulin homeostasis and insulin effectiveness or a perturbed acid-base buffer system with acid overload.
