Renal stone disease covers kidney and lower urinary tract stones caused by a variety of conditions, including metabolic and inherited disorders, and anatomical defects with or without chronic urinary infection. Most cases are idiopathic, in which there is undoubtedly a genetic predisposition, but where environmental and lifestyle factors play an important role. Indeed, it is becoming apparent that renal stone disease is often part of a larger ‘metabolic picture’ commonly associated with type 2 diabetes, obesity, dyslipidaemia, and hypertension. Renal stone disease is a growing problem in the UK (and other developed and developing populations) with a cross-sectional prevalence of ∼1.2%. This means that there are currently ∼720,000 individuals with a history of kidney stones in the UK. Almost 40% of first-time stone formers will form a second stone within 3 years of the first episode if no prophylactic measures are instituted to prevent stone recurrence, since removal or disintegration of the first stone does not treat the underlying cause of stones in the majority of patients. The age of onset is getting younger and the sex ratio (until recently more men than women) is becoming almost even. Metabolic screening remains an important part of investigating renal stone disease, but to the disappointment and frustration of many doctors, medical treatment is still essentially pragmatic, except perhaps in cystinuria, and to a limited extent in primary hyperoxaluria (if pyridoxine-sensitive); although newer treatments may be emerging. This review summarizes current thinking and provides a practical basis for the management of renal stone disease.

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Ten men with longstanding idiopathic Parkinson's disease (IPD) were investigated by urodynamic and electromyographic methods. The urodynamic studies were repeated after stopping anti-Parkinsonian medication for several hours. All patients showed a difference between the two studies, but the changes were unpredictable. Three patients who had high residual urine volumes in both studies were thought to have prostatic obstruction. EMG analysis showed no evidence of a lower motor neurone lesion affecting the striated urethral sphincter. It was concluded that micturition difficulty in the patient with IPD is due to detrusor hyperreflexia, influenced by the basal ganglia, which is not associated with impaired striated urethral sphincter activity.

Objective To evaluate whether injection with pericapsular lignocaine before transrectal ultrasonography (TRUS)-guided biopsy reduces the perceived pain of prostatic biopsy. Patients and methods The study included 121 patients referred for TRUS-guided biopsy of the prostate; 27 underwent biopsy with no previous injection and 94 were randomized to pericapsular injection with either 1% lignocaine or a placebo (saline). Both patient and operator were unaware of the content of the injection. The injection was delivered under TRUS guidance to the apex of the prostate. Routine sextant biopsies were taken using an 18 G needle in a spring-loaded biopsy gun. A validated pain scale, the NRS11 (0, no pain, to 10, unbearable pain), was used to record the pain of each biopsy.Results No significant placebo effect was detected between the 'no injection' and the placebo-injection group, with mean (95% confidence interval) pain scores of 3.58 (2.77-4.39) and 4.01 (3.46-4.51), respectively, using the unpaired Student's t -test ( P = 0.409). There was a statistically significant lower mean pain score in the lignocaine group, at 2.54 (2.00-3.10), than in the placebo-injection group ( P < 0.001). Conclusion Pericapsular injection with 1% lignocaine significantly reduces the perceived pain of TRUS-guided prostatic biopsy.