This study shows the high prevalence of marginal vitamin D nutrition in women in Saudi Arabia, which may predispose babies to rickets during infancy. In a country endowed with plentiful sunshine, the exclusion of sunshine by thick dark veils and bad housing probably contribute to this marginal state of vitamin D nutrition.The two major sources of vitamin D in the body are the diet and the skin. Dietary vitamin D is obtained from animal sources, and hence vegetarian diets are notorious for the lack of this vitamin.' The synthesis of vitamin D in the skin depends on exposure to ultraviolet rays from the sun2-4; the lack of sunshine in a country such as the UK can curtail exposure of the skin to the sun to an extent that people on vegetarian diets-for example, Asian immigrants in the UK-may develop a deficiency of vitamin D.5-8 This deficiency may be corrected spontaneously during the summer.9 It is, however, difficult to conceive of vitamin D deficiency in a setting where most people are non-vegetarian and where there is plentiful sunshine. It was therefore surprising that rickets was found frequently in preschool children in Saudi Arabia.In view of this finding we embarked on a study of vitamin D state in that section of the population of Saudi Arabia most vulnerable to lack of vitamin D-that is, the pregnant women and their newly delivered babies. Since the demands of vitamin D

The existence of nutritional deficiency rickets among infants in sunny Riyadh was confirmed radiologically. Most of the rachitic infants were breast-fed, some received unsupplemented infant feeding formulae, and all live in an environment that is devoid of sunlight. Their mean age at the time of onset was 10.5 months. 25-Hydroxyvitamin D (25OHD) levels were found to be low in mothers of the rachitic infants. This maternal deficiency as a factor in pathogenesis of rickets in the infant is discussed. Proposals are made to prevent the occurrence of rickets on this scale.

One hundred and twenty percutaneous renal biopsies performed in 104 patients aged 1 month to 15 years were analysed. Ultrasound examination was used for localization of the kidneys. Adequate renal tissue was obtained in 103 biopsies, with an overall success rate of 85.8%. The most frequent complication was gross haematuria, which occurred in 32 biopsies, but only 5 children required blood transfusion. Nineteen patients developed perirenal haematoma; 2 of these were symptomatic. Arteriovenous fistula was diagnosed in 2 patients. One patient died secondary to intestinal perforation. Serious complications were noted in patients with chronic renal failure. The success and complication rates in 10 patients less than 1 year of age were comparable with the rest of the group. The frequency of serious complications on renal biopsy in the present study was slightly higher than in the more developed countries.

We need to look out for cardiomyopathy among infants with hypocalcemia. For prevention maternal supplementation during pregnancy and lactation with up to 2000 units of vitamin D and 400 units for their infants.

Blood coagulation and platelet aggregation were assessed in children with nephrotic syndrome who were divided into the following groups: (1) relapse without treatment: (2) relapse on steroids; (3) early remission; (4) late remission and (5) steroid resistant. The renal histological findings were also recorded. Plasma anti-thrombin III (ATIII) levels were markedly reduced in groups 1 and 2, below normal in group 3 and were normal in groups 4 and 5. There was significant urinary loss of ATIII in groups 1 and 2 as well as in group 5. Plasma fibrinogen fluctuations exhibited the expected negative correlations with plasma ATIII. Reptilase time showed significant prolongation in groups 1, 2 and 3, and was near normal in groups 4 and 5. Platelet aggregation in response to arachidonic acid exhibited aggregation followed by disaggregation in groups 1, 2, 4 and 5, and was normal in group 3. Hyperaggregation in response to decreasing doses of ADP was noted in all patient groups as well as controls with no relationship to serum albumin levels. Aggregation responses to collagen and ristocetin were normal. It is concluded that: 1. The fluctuations in ATIII levels in childhood nephrotic syndrome are determined by the response to steroids and not by the renal histology per se. 2. An acquired fibrin polymerization defect (dysfibrinogenaemia) and an abnormality of the prostaglandin pathway of platelet activation, both reversible, are yet other haemostatic abnormalities in childhood nephrosis. 3. The discrepancies in the literature on haemostatic parameters, specially ATIII in childhood nephrosis, would not have arisen if their fluctuation in relation to steroid therapy as well as the renal histological features of nephrotic syndrome had been documented simultaneously.