Case report 17p11-q21 [2]. Hypercalciuria has occasionally been reported [3]. The condition has been diagnosed from age A 40-year-old man was referred with hypertension and microscopic haematuria. His mother and sister had 2 weeks to adulthood. The primary lesion is increased chloride reabsorption in the ascending loop of Henle, Gordon's syndrome. His blood pressure was 190/115 mmHg, his potassium 6.0 mmol/L, creatinine leading to inhibition of the renin-aldosterone axis. Lack of sodium in the distal convoluted tubule, with a relative 87 mmol/L, bicarbonate 21 mmol/L and calcium 2.29 mmol/L. IVU and ultrasonography showed a 4 cm hypoaldosteronism, leads to decreased potassium secretion. Hypertension is caused by increased total body stone in the left kidney. The stone was treated successfully with combined ESWL and percutaneous nephrolisodium stores. To our knowledge, this is the first reported case of recurrent renal calculus formation in Gordon's thotomy with ultrasonic disintegration. Analysis confirmed a mixed calcium oxalate and phosphate stone.syndrome. The syndrome is probably more prevalent than the literature suggests. Renal stones, hyperkalaemia Investigation showed hypercalciuria at 11.4 mmol/24 h and normal urinary oxalate, cystine and citrate; the and hypertension in the presence of a normal serum creatinine should raise the possibility. Life-long therapy urinary pH was 6.6. Creatinine clearance was normal (95 mL/min), and recumbent and ambulant renin with thiazide diuretics is eCective in controlling all the main features. plasma levels were both 0.30 ng/mL per hour (normal levels 0.98-4.18 and 0.51-2.64, respectively). The aldosterone recumbent and ambulant levels were 137 and 120 pg/mL, respectively (normal level both no stone recurred within 9 months. His urinary calcium J Pediatr 1974; 85: 355-8 excretion rate reduced dramatically to 2.50 mmol/24 h; at his own insistence, he remains on a low-calcium diet.

It seems that mental health services in this country have reached the point where resistance to change should be crumbling in the face of perceived failure to deliver the required services. Whilst it could be argued that a major and potent source of internal change is performance gaps, few things force change more than sudden and unexpected information about poor organizational performance.

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