Biochemical and Morphological Aspects of Bone Tissue in Chronic Renal Failure

Self Cite

In chronic uremia, the clinical disorders of calcium and phosphorus metabolism are nfluenced by the following factors: (1) intestinal absorption of calcium and phosphate, resulting in a negative calcium and phosphate balance at normal dietary intakes; (2) renal handling of calcium and phosphate: the fractional transport of calcium (the isoosmotic reabsorption taking place in the proximal tubule) is not affected by GFR modifications, whereas the Tm-limited reabsorption is severely impaired; the external phosphate balance is kept, even in the presence of a reduced nephron population, by means of a proportional reduction in Tmpo₄ values; physicochemical state and turnover of body calcium and phosphate: in uremic patients, the distribution spaces, turnover rate of calcium, and accretion rate of bones are increased in comparison with the controls; the calcium infusion test in patients with renal osteomalacia is followed by a regular increase in plasma [PO₄], whereas a significant decrease is observed in patients with renal osteitis fibrosa, due to the extreme ‘avidity’ of bones for calcium phosphate; the role of hyperphosphatemia is critical in keeping the plasma [Ca] lower than the expected values for a given metabolic set; moreover, an increased cell uptake of phosphate could counteract to some extent the reduced renal clearance of phosphate; structural and biochemical modifications of bone tissue: uremic osteodystrophy consists mainly of two components: (a) osteomalacia, with osteoid excess, disappearance of the calcification front, and diffuse pathologic mineralization, and (b) osteitis fibrosa, with severe resorption of normally mineralized bone, slight osteoid excess, and almost normal calcification front; (5) hormonal factors: chronic stimulation of parathyroid glands may result in suppressible or even autonomous hyperparathyroidism. As to vitamin D, it has been suggested that the uremic kidney is not able to synthesize the 1,25-di-OH-cholecalciferol, the active metabolite of vitamin D: this results in an impaired intestinal absorption of calcium. On the contrary, the role of calcitonin in chronic uremia is still uncertain, since low values of plasma [Ca] are usually observed.

Section: Renal Handling O F Calcium and Phosphatesupporting

confidence: 83%

Calcium and Phosphorus Metabolism in Chronic Uremia

Fiaschi¹,

Mioni²,

Maschio³

et al. 1975

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“…On the other hand, it cannot be ex cluded that the enzyme system involved in the synthesis of l,25-(OH)2-cholecalciferol may have been damaged as a consequence of ex tensive tubular lesions which are usually ob served in obstructive nephropathy [7], 29% of patients with mild renal in sufficiency were found to have an association of osteomalacia and osteoclastic bone resorp tion. This percentage is significantly higher than that previously observed in patients with severe chronic renal failure of diverse etiology [17]. It has been claimed that the hypercal- ciuria, which is usually observed in 30-40% of patients with nephrolithiasis [14,29], could lead, by unknown pathways, to secondary hyperparathyroidism [9], In our experience, hypercalciuria was actu ally observed in 35.7% of patients with normal GFR, but without any correlation with mor phological evidence of hyperparathyroidism.…”

Section: Commentcontrasting

confidence: 45%

“…Bone biopsies were taken from the iliac crest under local anesthesia by using a trephine allowing 5 mm dia meter and 14-18 mm long specimens (S. Orsola needle, Bologna, Italy) [17], All patients were fully aware of the nature of the investigation and gave their consent to the biopsy.…”

Section: Bone Biopsy Studymentioning

confidence: 99%

Aspects of Calcium Metabolism in Obstructive Nephropathy

Maschio

D’Angelo

Bonucci

et al. 1977

Self Cite

In 28 patients with bilaterally recurring calcium – containing renal staghorn calculi, 14 with normal GFR and 14 with mild renal insufficiency, a metabolic investigation of calcium metabolism during intravenous phosphate loading and a morphologic (optical and electron microscopic) study by means of percutaneous bone biopsy were performed. The morphologic investigation showed evidence of osteomalacia in 28.5% of the patients with normal GFR and in 50% of those with renal insufficiency. Moreover, histological evidence of hyperparathyroidism was found in an additional 29% of the patients with renal insufficiency. The metabolic investigation demonstrated low values of Tm PO₄/GFR only in patients with morphologic evidence of hyperparathyroidism. Moreover, the fall in plasma calcium concentration during phosphate loading appeared to be more evident and significant in patients with osteodystrophy than in those with normal bone. It is possible that the disordered vitamin D metabolism in patients with renal insufficiency and the renal parenchymal lesions observed in all of the patients may have played some role in the pathogenesis of osteomalacia, while the repeated insults to the kidney secondary to ureteropelvic obstructions may have led to early secondary hyperparathyroidism. From the metabolic point of view, our results support the validity of phosphate infusions in assessing the Tm PO₄/GFR as a functional index of hyperparathyroidism, and the exaggerated fall in plasma calcium concentration as an index of metabolic bone disease.

“…It consists of features of osteo malacia, osteitis fibrosa, osteosclerosis and osteoporosis, the first two being the more important [1]. There are two major mecha nisms involved in the development of renal bone disease: parathyroid hormone oversecre tion [2,3], and disturbances in the vitamin D metabolism [4], which requires a renal trans formation to its active metabolite 1,25-dihydroxycholecalciferol [5].…”

Section: Introductionmentioning

confidence: 99%

Metacarpal Cortical Thickness in Uremic Patients on Regular Hemodialysis

Río¹,

Rico²,

Carrera³

et al. 1978

Metacarpal cortical thickness was measured in 83 patients with chronic renal failure undergoing periodic hemodialysis. Patients were dialyzed twice weekly, 8–9 h per session, with a calcium concentration in dialysate of 6.5 mg/dl. Supplements of calcium, vitamin D (5,000 I.U. a day), steroid anabolic hormones, and aluminium hydroxyde were administered to all patients. They were on a normal protein intake and unrestricted physical activity. The results show that the young males have a reduction in cortical thickness as compared to age-matched controls, and that there is a progressive loss in cortical width as the length of dialysis increases. This bone loss is statistically significant in males during their first 18 months of dialysis.