Assessment and Management of Urinary Dysfunction in 187 Patients with Parkinson's Disease.

BACKGROUND: Urinary dysfunction is common in Parkinson's disease (PD) patients and management options are limited. OBJECTIVE: This study aimed to explore the management of urinary dysfunction by researching the special needs of PD patients. METHODS: PD patients with urinary dysfunction who underwent urodynamic testing were recruited from a single center from October 2013 to February 2019. The urinary symptoms, International Prostate Symptom Score and Hoehn-Yahr scale were evaluated. Management was made at the urologists' discretion with follow-up after three weeks. Urinary symptoms, urodynamics and the management of urinary dysfunction were analyzed. RESULTS: A total of 187 patients with a median age of 66.2 and Hoehn-Yahr scale soccer of 2 were enrolled. Irritative symptoms were more common than obstructive symptoms, while obstructive symptoms were more common in male than female patients, except for incomplete voiding. There were 51% cases of detrusor overactivity, followed by 33% with bladder outlet obstruction, 13% had normal function, 12% had detrusor underactivity, 9% had stress incontinence, 7% had increased bladder sensation and 4% had an acontractile bladder. Tolterodine and tamsulosin were the most common therapeutic agents, respectively prescribed to 38.5% and 27.3% of the patients. Other treatments included catheterization, botulinum toxin A bladder wall injection, transurethral resection of the prostate and urethral dilatation. Urinary symptoms were improved significantly in 74.5% of the patients (p < 0.001), including 27 patients treated with tamsulosin only and 54 patients with tolterodine only. CONCLUSIONS: Urinary symptoms and urodynamics were highly variable in PD patients, indicating that most patients may benefit from personalized management.

Studies on the protective effect of dietary fish oil on gentamicin-induced nephrotoxicity and oxidative damage in rat kidney.

Gentamicin (GM)-induced nephrotoxicity limits its long-term clinical use. Several agents/strategies were attempted to prevent GM nephrotoxicity but were not found suitable for clinical practice. Dietary fish oil (FO) retard the progression of certain types of cancers, cardiovascular and renal disorders. We aimed to evaluate protective effect of FO on GM-induced renal proximal tubular damage. The rats were pre-fed experimental diets for 10 days and then received GM (80 mg/kg body weight/day) treatment for 10 days while still on diet. Serum/urine parameters, enzymes of carbohydrate metabolism, brush border membrane (BBM), oxidative stress and phosphate transport in rat kidney were analyzed. GM nephrotoxicity was recorded by increased serum creatinine and blood urea nitrogen. GM increased the activities of lactate and glucose-6-phosphate dehydrogenases whereas decreased malate, isocitrate dehydrogenases; glucose-6 and fructose-1,6-bisphosphatases; superoxide dismutase, catalase, glutathione peroxidase and BBM enzymes. In contrast, FO alone increased enzyme activities of carbohydrate metabolism, BBM and oxidative stress. FO feeding to GM treated rats markedly enhanced resistance to GM elicited deleterious effects and prevented GM-induced decrease in 32Pi uptake across BBM. Dietary FO supplementation ameliorated GM-induced specific metabolic alterations and oxidative damage due to its intrinsic biochemical/antioxidant properties.

Characterization of magnesium-induced urinary disease in the cat and comparison with feline urologic syndrome.

Aggregates of struvite crystals caused urethral obstruction in a high percentage of cats fed moist and dry diets supplemented with Mg oxide. Some of the diets were associated with cystolith formation as well. The percentage of Mg in the experimental diets was a misleading indicator of Mg intake because of differences between moist and dry diets in their caloric density. Magnesium homeostasis was maintained in cats ingesting large quantities of Mg. Tissue (kidney, muscle, and rib) concentrations of Mg were the same in cats fed high Mg and control diets. Plasma Mg concentration was increased only in cats ingesting the largest amount of Mg. Magnesium homeostasis was maintained by a marked increase in urine Mg excretion. However, urine Mg concentration was not directly related to Mg intake, apparently because of differences between diets in intestinal absorption of Mg. Urethral obstruction of experimental cats was not associated with a transient increase in Mg intake, nor did obstructing cats have higher urine Mg concentrations than did nonobstructing cats fed the same diet. This observation indicates that factor(s) other than urine Mg concentration are important in urethral obstruction. Cats with urethral obstruction due to naturally occurring disease, feline urological syndrome (FUS), had markedly lower urine Mg concentrations than cats fed high Mg diets. This finding refutes the theory that cats develop FUS because of primary Mg hyperabsorptive phenomena or because of a primary urinary leak of Mg. It also indicates that factors other than urine Mg concentration are involved in the genesis of naturally occurring urethral obstruction. Another difference between the natural and the induced disease was related to the character of the urinary precipitates. Experimental diets higher in Mg concentration caused urolith formation, which is uncommon with FUS. Lower Mg diets caused obstruction with aggregates of crystals, but mucus was not observed. However, in the experimental disease induced in the present study, urinary precipitates were predominantly or exclusively struvite, as has been reported in the natural disease. Many similarities were seen between the diet-induced disease and FUS, but factors in addition to Mg intake are involved in the natural disease. The importance of Mg, compared with the undefined factors, remains to be established.