Rheumatic manifestations of renal disease

Two diseases associated with chronic kidney disease (CKD) have benefited from advances in the past year which are of great importance for rheumatologists: renal osteodystrophy, which is now clearly associated with vascular calcification and cardiovascular death, and nephogenic systemic fibrosis, which appears presently as a new iatrogenic disorder, and therefore can be prevented.

Vascular calcification is a feature of renal osteodystrophy, which has received much recent attention. Hyperphosphatemia has been shown to play an important role by inducing a transcription factor, osterix, which promotes the transformation of vascular smooth muscle cells into osteoblats-like cells and matrix calcification. The effect of calcium load on vascular calcification is modulated by bone turnover. Calcium has been found to promote more vascular calcification in adynamic bone disease in which bone cannot act anymore as a buffer for absorbed calcium.

Management of renal osteodystrophy is progressing relentlessly, in particular, since the discovery of new phosphate binders, vitamin D derivates and calcium agonist. The need to maintain serum parathyroid hormone to levels higher than the normal range has been emphasized in CKD patients, who early develop skeletal resistance to the hormone. However, bone turnover has been found excessively suppressed in dialysis patients whose serum parathyroid hormone levels met the recommended values, reflecting imperfections in the assays presently used in clinical practice.Nephrogenic systemic fibrosis has been linked to exposition of CKD patients to gadolinium-based contrast agents, by epidemiological and experimental data. Avoidance of gadolinium - in particular gadodiamide - enhanced MRI in CKD patients, now appears as an efficient way to prevent this very serious disease.