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The World Kidney Day offers a crucial opportunity to the Belgian associations of nephrologists to inform public and medical communities about the global problem of chronic kidney disease (CKD). According to epidemiological data from GNFB/ NBVN registries in our country, cardiovascular diseases and diabetes 2 are responsible for an increasing amount of CKD cases with pejorative evolution to end-stage renal disease requiring cost-effective renal replacement therapies (haemodialysis, peritoneal dialysis or renal transplantation). In these patients, the high level of comorbidities and the late referral to the nephrologists are recognized as enhanced morbidity and mortality factors. These facts underline the need for the nephrologists to stimulate collaboration with general practitioners and specialists from other disciplines in order to set up systematic screening procedures and early follow-up of patients at risk of developing CKD. These procedures should contribute to reduce the progression rate of renal function impairment.

Acitretin (Ro 10-1670 or Neotigason), a free acid and the main metabolite of etretinate (Ro 10-9359 or Tigason), is the most recent of the retinoids used orally in the treatment of psoriasis and numerous other dermatoses exhibiting disorders of keratinization. In the majority of cases, its side-effects are similar to those of hypervitaminosis A.

These recommendations are largely based on the Executive Summary of the "European Guidelines on Cardiovascular Disease Prevention in Clinical Practice" proposed by the "Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice". The model used to assess the overall risk was adapted for Belgium. Otherwise, very few things were changed from the Executive Summary of the European Guidelines.

These recommendations are largely based on the Executive Summary of the "European Guidelines on Cardiovascular Disease Prevention in Clinical Practice" proposed by the "Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice". The model used to assess the overall risk was adapted for Belgium. Otherwise, very few things were changed from the Executive Summary of the European Guidelines.

These recommandations are largely based on the "European Guidelines on Cardiovascular Disease Prevention in Clinical Practice" proposed by the "Third Joint Task Force of European and other Societies on Cardiovascular Disease Prevention in Clinical Practice". The model used to assess the overall risk was adapted for Belgium. Otherwise, very few things were changed from the Exectutive Summary of the European Guidelines.

Acitretin (Ro 10-1670 or Neotigason), a free acid and the main metabolite of etretinate (Ro 10-9359 or Tigason), is the most recent of the retinoids used orally in the treatment of psoriasis and numerous other dermatoses exhibiting disorders of keratinization. In the majority of cases, its side-effects are similar to those of hypervitaminosis A.

Tumor-induced osteomalacia is due to renal phosphate wasting in response to a humoral factor produced by a tumor, usually a benign mesenchymal tumor. Removal of the tumor is followed by resolution of the metabolic disorder. Physicians should be aware that sporadic renal phosphate wasting in an adult should prompt a search for a tumor. A case of tumor-induced osteomalacia due to a nonossifying fibroma of the radius is reported. After removal of the tumor, renal phosphate excretion returned to normal, but the patient developed tertiary hyperparathyroidism. Eight years elapsed between symptom onset and the diagnosis of the tumor. The pathogenesis of tumor-induced osteomalacia and the role of treatment for renal phosphate wasting on the subsequent development of hyperthyroidism are discussed.

We have shown that administration of inorganic potassium phosphates (Pi) to patients with severe diabetic ketoacidosis was able to increase the P50 (the PO2 necessary to achieve a hemoglobin saturation of 50%) by a non diphosphoglycerate (DPG) mediated effect. This suggests that the oxyhemoglobin dissociation curve (ODC) may be determined not only by pH, temperature, CO2 content and DPG but also by plasmatic ions. In order to test this hypothesis we have determined the ODC on whole blood in two groups of subjects, 49 control subjects with matching age and sex and 49 patients suffering from liver cirrhosis, acute pancreatitis, septic shock and acute respiratory distress syndrome. The patients had many ionic disorders induced either by their diseases or by the applied treatment. The mean ODC of the patients did not differ from the normal values. In contrast, the dispersion of PO2 around the saturations values was increased from 5 to 80% saturation. A forward regression analysis showed that the DPG level and the levels of inorganic phosphates and natrium (Na+) played a significant role in determining the position of the ODC according to the following equation: P50 (mmHg) = 34.5 + 0.225 DPG + 0.62 Pi-0.09 Na+, where DPG is in micromol.gHb-1 and Pi and Na+ in mEq.l-1. In separate experiments we showed that the Bohr effect as expressed in d (log PO2)/dpH amounted to -0.53, -0.46 and -0.42 for SO2 equal to 5%, 50% and 95%, respectively. The corresponding values for the temperature effect was expressed in d (log PO2)/dT amounted to 0.028, 0.024, and 0.020 respectively. The fact that ions play an role in regulating the position of the ODC of patients with ionic disorders may have therapeutical implications, preventive or curative.

The wide spectrum of inherited glomerular diseases can be classified in four groups, as indicated in table 3–1. The genetic information available varies from one disease to another. In some conditions, such as Fabry’s disease, the enzyme defect has long been identified, there are biochemical methods for early diagnosis, and DNA technology is being used to determine the molecular gene defect(s). In other conditions, such as Alport’s syndrome and its variants, although clinical and genetic heterogeneity is well established, the antigenic defect of the glomerular basement membrane (GBM) has just been identified, and DNA analysis has been initiated only in the X-linked form. Lastly, in many cases such as primary familial glomerulonephritides, which are often sporadic and where familial aggregation has rarely been documented, genetic information is scarce. Yet these familial cases are of great interest because they illustrate how crucial genetic factors are in primary glomerular diseases. They also provide an opportunity to review the methodology that should be used to demonstrate genetic predisposition in polygenic diseases.

Progressive hereditary nephritis is subdivided into Alport's syndrome (with extrarenal involvement) and hereditary nephritis without deafness. Three modes of inheritance have been described: X-linked dominant, autosomal dominant, and autosomal recessive. We reviewed the mode of inheritance in 48 kindred with hereditary nephritis (41 with Alport's syndrome and 7 with hereditary nephritis without deafness). It was presumed X-linked dominant in 34 Alport's syndrome and 6 hereditary nephritis without deafness, autosomal dominant in five hereditary nephritis and one hereditary nephritis without deafness, and autosomal recessive in two Alport's syndrome. We studied the cumulative renal survival of 149 patients, 128 (76 males, 52 females) with Alport's syndrome and 21 (10 males, and 11 females) with hereditary nephritis without deafness. Major prognostic factors were the patient's sex (median renal survival in males and females being respectively 32 versus 61 years in Alport's syndrome and 34 versus 57 years in hereditary nephritis without deafness), and the mode of inheritance (median renal survival in males being 25 years in X-linked dominant Alport's syndrome versus 51 years in autosomal dominant Alport's syndrome). The presence of hearing loss in the kindred or in the patient himself did not appear as a significant prognostic factor. We conclude that Alport's syndrome and hereditary nephritis without deafness are predominantly X-linked dominant diseases with the same renal outcome, and that in Alport's syndrome the patient's sex and the mode of inheritance are two independent prognostic factors.

Glomerulonephritis (GN) due to antiglomerular basement membrane (GBM) antibodies after kidney transplantation may be classified into two groups: 1. Recurrent GN are very rare provided circulating anti-GBM antibodies are absent at grafting. If present, linear fixation along the GBM occurs but does not lead to GN in some cases. 2. De novo anti-GBM diseases have been rarely reported. They developed in 8 patients with Alport's syndrome and in at least 3 additional patients in whom hereditary nephritis was not the original disease. A prospective and retrospective study was performed in 54 transplanted patients with hereditary nephritis: circulating anti-GBM antibodies were detected in only one case; linear fixation along the GBM was found but no evidence of GN. The risk of anti-GBM disease after kidney transplantation is low in patients with hereditary nephritis but this complication must be rapidly identified. Its occurrence is probably related to the defect in GBM antigenicity involving the Goodpasture antigen, found in some patients with Alport's syndrome or related hereditary nephritis.

Progressive hereditary nephritis is subdivided into Alport's syndrome (with extrarenal involvement) and hereditary nephritis without deafness. Three modes of inheritance have been described: X-linked dominant, autosomal dominant, and autosomal recessive. We reviewed the mode of inheritance in 48 kindred with hereditary nephritis (41 with Alport's syndrome and 7 with hereditary nephritis without deafness). It was presumed X-linked dominant in 34 Alport's syndrome and 6 hereditary nephritis without deafness, autosomal dominant in five hereditary nephritis and one hereditary nephritis without deafness, and autosomal recessive in two Alport's syndrome. We studied the cumulative renal survival of 149 patients, 128 (76 males, 52 females) with Alport's syndrome and 21 (10 males, and 11 females) with hereditary nephritis without deafness. Major prognostic factors were the patient's sex (median renal survival in males and females being respectively 32 versus 61 years in Alport's syndrome and 34 versus 57 years in hereditary nephritis without deafness), and the mode of inheritance (median renal survival in males being 25 years in X-linked dominant Alport's syndrome versus 51 years in autosomal dominant Alport's syndrome). The presence of hearing loss in the kindred or in the patient himself did not appear as a significant prognostic factor. We conclude that Alport's syndrome and hereditary nephritis without deafness are predominantly X-linked dominant diseases with the same renal outcome, and that in Alport's syndrome the patient's sex and the mode of inheritance are two independent prognostic factors.