Diffuse hepatocellular calcification developing in a patient on chronic hemodialysis after ischemic hepatitis

Diffuse hepatic calcification is a rare condition. Previous reports have described patients with end-stage renal disease who developed diffuse hepatic calcification after ischemic hepatitis caused by shock. We herein present a similar case. A 41-year-old man on chronic hemodialysis developed ischemic hepatitis due to shock induced by ventricular tachycardia, followed by progressive hepatic failure. Necropsy of the liver revealed diffuse hepatocellular calcification. Given the similarity by which our case and previously reported cases developed this rare condition, we postulate that chronic renal failure is involved in the pathogenesis of diffuse hepatic calcification.     

Early detection of heart transplant patients with increased risk of ciclosporin nephrotoxicity

Chronic nephrotoxic effects from ciclosporin are a common clinical complication after heart transplantation and frequently lead to progressive renal failure. There is no laboratory test to predict development of chronic renal failure in heart transplant patients. We analysed urinary retinol-binding protein (uRBP) concentration, to assess proximal tubular dysfunction, in 36 clinically stable heart transplant patients. We detected a subgroup of 13 patients who had high concentrations of uRBP, good renal function, and a high risk of developing progressive renal failure compared with patients with normal uRBP (relative risk 3.87, p=0.003).     

Calcium metabolism in renal failure

Osteodystrophy is almost universally present in chronic renal failure. Mild, but detectable, abnormalities—especially in parathyroid hormone (PTH) secretion—occur even when the glomerular filtration rate is greater than 30 cc/min. Osteomalacia is common in areas in which vitamin D intake and exposure to sunlight are minimal; when these factors are plentiful, osteitis fibrosa predominates. Osteoporosis is seen with increasing frequency in hemodialyzed patients. Nonosseous complications of secondary hyperparathyroidism include hypercalcemia, metastatic calcification and pruritus. The most important factor in the medical therapy of Osteodystrophy is control of serum phosphate levels. Next, a positive calcium balance must be provided either by giving vitamin D as dihydrotachysterol, raising dialysate calcium or administering calcium orally. Parathyroidectomy is sometimes indicated, especially when the patients are transplant candidates and manifest hypercalcemia. Whether or not transplant is contemplated, patients with persistently high calcium-phosphate products, severe metastatic calcification or rapidly progressive Osteodystrophy should be considered for parathyroidectomy. Newer, experimental vitamin D preparations, such as 1,25-dihydroxycholecalciferol or 1-alpha-hydroxycholecalciferol, should improve the management of patients with renal Osteodystrophy and decrease the need for parathyroidectomies.     

Extensive metastatic calcification of the lung in an azotemic patient

An unusual case of extensive pulmonary metastatic calcification occurring during the course of chronic pyelonephritis is described. The important features of this case are as follows: (1) Metastatic calcification appeared to develop in an early state of chronic renal failure when there was neither hypercalcemia, hyperphosphatemia, hyperparathyroidism nor evidence of bone disease. (2) The calcium and phosphate ion product was normal during the last 3 years when the pulmonary metastatic deposits persisted and progressed with the roentgenologic appearance of pulmonary edema. (3) There was calcium carbonate rather than the anticipated calcium phosphate in the deposited material. A review of the literature offers some theoretic explanation for the sites of calcification but no practical explanation for the presence of calcification.     

Infective endocarditis with extensive calcified granulation of the mitral annulus and valve--a case report

Mitral annular calcification, a degenerative process usually seen in the elderly or in chronic renal failure, is rarely seen in an extensive form. A 69-year-old man with no history of renal failure, rheumatic fever, or heart disease had mitral valve vegetation and regurgitation, together with extensive mitral annuls and valve calcification, which may or may not have been secondary to the infective endocarditis.     

Chronic rejection of renal transplants: new clinical insights

Chronic rejection is the most important cause for returning to dialysis after failure of a renal transplant. The term chronic allograft nephropathy refers to the progressive decline of renal function seen in some renal transplant recipients in association with alloantigen-dependent and alloantigen-independent factors. This review examines the role of factors related to allorecognition, injury, nephron dosing, and donor and recipient characteristics in the development of chronic allograft nephropathy. The clinical associations to chronic allograft nephropathy are presented in the context of pathogenetic mechanisms of renal damage and disease progression. As there is no therapy available at this time for established chronic allograft nephropathy, possible areas of intervention for the prevention of chronic rejection are discussed.     

慢性肾衰竭血管钙化与高磷血症

血管钙化和高磷血症是慢性肾衰竭患者心血管疾病发生率高、死亡率高的主要危险因素。高磷血症对慢性肾衰竭血管钙化起重要作用。     

Calcium deposition with or without bone formation in the lung

Pulmonary calcification and ossification occurs with a number of systemic and pulmonary conditions. Specific symptoms are often lacking, but calcification may be a marker of disease severity and its chronicity. Pathophysiologic states predisposing to pulmonary calcification and ossification include hypercalcemia, a local alkaline environment, and previous lung injury. Factors such as enhanced alkaline phosphatase activity, active angiogenesis, and mitogenic effects of growth factors may also contribute. The clinical classification of pulmonary calcification includes both metastatic calcification, in which calcium deposits in previously normal lung or dystrophic calcification, which occurs in previously injured lung. Pulmonary ossification can be idiopathic or can result from a variety of underlying pulmonary, cardiac, or extracardiopulmonary disorders. The diagnosis of pulmonary calcification and ossification requires various imaging techniques, including chest radiography, computed tomographic scanning, and bone scintigraphy. Interpretation of the presence of and the specific pattern of calcification or ossification may obviate the need for invasive biopsy. In this review, specific conditions causing pulmonary calcification or ossification that may impact diagnostic and treatment decisions are highlighted. These include metastatic calcification caused by chronic renal failure and orthotopic liver transplantation, dystrophic calcification caused by granulomatous disorders, DNA viruses, parasitic infections, pulmonary amyloidosis, vascular calcification, the idiopathic disorder pulmonary alveolar microlithiasis, and various forms of pulmonary ossification.     

Calcific stenosis of a mitral valve xenograft in a patient in chronic renal failure

A 61 year old man presented with mitral regurgitation and glomerulonephritis caused by suspected infective endocarditis. His glomerulonephritis remitted on immunosuppression but mitral valve replacement with a Carpentier-Edwards porcine xenograft later proved necessary. The patient became dialysis dependent and cadaveric renal allografting was complicated by delayed graft function and refractory pulmonary oedema. Cardiac catheterisation showed severe calcification and stenosis of the xenograft with a transvalvar gradient of 23 mm Hg and despite emergency valve replacement the patient died. The valve had been in place less than five years. The rapid calcification and stenosis of a bioprosthetic heart valve calls into question the use of such prostheses in patients with chronic renal failure.     

Calcific stenosis of a mitral valve xenograft in a patient in chronic renal failure.

A 61 year old man presented with mitral regurgitation and glomerulonephritis caused by suspected infective endocarditis. His glomerulonephritis remitted on immunosuppression but mitral valve replacement with a Carpentier-Edwards porcine xenograft later proved necessary. The patient became dialysis dependent and cadaveric renal allografting was complicated by delayed graft function and refractory pulmonary oedema. Cardiac catheterisation showed severe calcification and stenosis of the xenograft with a transvalvar gradient of 23 mm Hg and despite emergency valve replacement the patient died. The valve had been in place less than five years. The rapid calcification and stenosis of a bioprosthetic heart valve calls into question the use of such prostheses in patients with chronic renal failure.     

Calcification in nonfunctioning transplanted kidneys

Failed renal allografts often are left in situ in patients who revert to chronic dialysis therapy or who undergo retransplantation. These organs may be the site of massive calcification despite their lack of physiological function. Calcification of an endstage renal allograft is sometimes found incidentally. We report here two patients who developed extensive calcification of the renal graft, one was on chronic hemodialysis and the other had a second renal transplantation with normal renal function. The precise pathogenesis of calcification and the factors which determine its tissue localization are unclear. Factors postulated to promote the development of metastatic calcification include an elevated calcium phosphate product, severe secondary hyperparathyroidism, aluminium toxicity and duration of dialytic therapy. In some cases local factors related with the chronic inflammatory rejection process are probably involved as well. However, the exact relative contribution of these factors remains unresolved. Unless specific clinical indications are present, transplant nephrectomy is not necessary for calcified end-stage renal allografts.     

Chronic kidney disease: effects on the cardiovascular system

Accelerated cardiovascular disease is a frequent complication of renal disease. Chronic kidney disease promotes hypertension and dyslipidemia, which in turn can contribute to the progression of renal failure. Furthermore, diabetic nephropathy is the leading cause of renal failure in developed countries. Together, hypertension, dyslipidemia, and diabetes are major risk factors for the development of endothelial dysfunction and progression of atherosclerosis. Inflammatory mediators are often elevated and the renin-angiotensin system is frequently activated in chronic kidney disease, which likely contributes through enhanced production of reactive oxygen species to the accelerated atherosclerosis observed in chronic kidney disease. Promoters of calcification are increased and inhibitors of calcification are reduced, which favors metastatic vascular calcification, an important participant in vascular injury associated with end-stage renal disease. Accelerated atherosclerosis will then lead to increased prevalence of coronary artery disease, heart failure, stroke, and peripheral arterial disease. Consequently, subjects with chronic renal failure are exposed to increased morbidity and mortality as a result of cardiovascular events. Prevention and treatment of cardiovascular disease are major considerations in the management of individuals with chronic kidney disease.     

Calcified small cell carcinoma of the lung

Calcification within pulmonary lesions usually signifies a benign entity, but depending on the specific pattern of calcification it can also represent malignancy. The authors report a case of calcified small cell lung cancer in a patient with end-stage renal disease. The calcification was unrelated to renal failure and not the result of metastatic calcification, and the pattern of calcification and tissue pathology excluded other causes of calcification within this mediastinal mass.     

Calciphylaxis associated with rheumatoid arthritis: communication of the second case

Calciphylaxis is the tissue sensitivity to calcification, described mainly in patients with chronic renal insufficiency, renal transplant of parathyroid dysfunction. There is only one case described in a patient with rheumatoid arthritis, without renal dysfunction, nor hyperparathyroidism. We present the second case in a woman with inactive rheumatoid arthritis.     

Mönckeberg's sclerosis: an unusual presentation--a case report

Calcification of the media of peripheral arteries is referred to as M?nckeberg's sclerosis and occurs commonly in aged individuals. However, it also occurs in younger patients with diabetes mellitus and chronic renal failure. In diabetic patients, medial calcification appears to be a strong independent predictor of cardiovascular mortality. In this report, we have presented a 20 year-old-patient with extensive peripheral artery calcification. The etiology of calcification was not identified. It has been suggested that this was an unusual form of M?nckeberg's sclerosis.     

Calcification and degeneration following mitral valve reconstruction in patients requiring chronic dialysis

BACKGROUND AND AIM OF THE STUDY: Abnormal calcium homeostasis in patients with end-stage renal failure results in dystrophic calcification; this limits the use of heterograft tissue valve prostheses in patients on chronic dialysis. Mitral valve reconstruction offers advantages over mitral replacement in many patients without renal failure, and offers theoretical advantages in patients requiring dialysis. This study was performed to determine the outcome of mitral valve reconstruction in patients with renal failure requiring chronic dialysis. METHODS: Ten patients with end-stage renal failure and on chronic dialysis who underwent mitral valve repair were identified retrospectively and followed for clinical and echocardiographic outcome. All patients had good results immediately following surgical valve mitral repair, with no more than mild mitral regurgitation and low transmitral gradients on intraoperative transesophageal echocardiography. RESULTS: Clinical and echocardiographic follow up was available for eight patients at an average of 2.3 +/- 1.4 years after surgery. Despite there being no significant valve calcification at the time of surgery, visible mitral leaflet calcification was evident in seven of these patients, and the transmitral gradient for the group was significantly increased (from 4.8 +/- 1.7 mmHg to 8.3 +/- 3.9 mmHg, p = 0.04). Two patients required reoperation for failed mitral repair; one at six months due to chordal rupture, and one at 15 months due to mitral calcification with stenosis. CONCLUSION: Despite good early surgical results, there was accelerated calcification of the repaired mitral valve, a rapid increase in postoperative mitral gradients, and a high incidence of failure of the reconstruction. Additional prospective studies are required to evaluate the optimal intervention for patients with end-stage renal failure who require mitral valve surgery.     

Transient postoperative pericardial constriction in a child

Constrictive pericarditis has been defined classically as a progressive condition, characterized by pericardial fibrosis, with or without calcification, which results in chronic refractory congestive heart failure and for witch pericardiectomy is often required. In the last decades there have been reports describing a transient form of constrictive pericarditis, which resolves without surgical therapy. This "fibroelastic form" would represent the acute or subacute phase of constriction. In many patients, pericardial inflammation continues and pericardial fibrosis and calcification develop, leading to a chronic and rigid constrictive pericarditis. However, in some patients, pericardial inflammation resolves without progressing to chronic constrictive pericarditis. We report a 7 year old boy, who developed clinical and echocardiographical findings of pericardial constriction 5 weeks after a cardiac surgery, which resolved with steroid therapy.     

Viral hepatitis C in patients with renal disease

Hepatitis C in patients with chronic renal failure. Infection with hepatitis C virus (HCV) is a common complication in those patients under chronic dialysis. Prevalence varies from 8% to 65 percent. Immunization against hepatitis A and B for renal patients is always recommended, especially in countries with high prevalence of this type of hepatitis. Interferon as the only antiviral treatment is recommended for patients with chronic renal failure and chronic hepatitis who depend on dialysis. Viral hepatitis is the first cause of morbidity and mortality among renal recipients. Prevalence varies between 4 and 38%, depending on the geographic area. Infection with HCV usually begins before the transplant, although the patient is sometimes infected during the transplant because the donor organs carry the virus. The chronic HCV infection dosen't seem to affect the survival rate of the patient or the organ, compared to the survival rate in patients without the infection. Chronic hepatitis C without cirrhosis is not a contraindication for renal transplant, but cirrhosis is. Liver failure is the cause of death in 8-28% of renal transplant recipients infected with hepatitis C virus.     

Resolution of breast pain and calcification with renal transplantation.

Vascular calcification in chronic renal failure and dialysis patients is well-documented and generally considered to be a consequence of decreased phosphorus excretion, secondary hyperparathyroidism, and increased calcium-phosphorus product. Following renal transplantation or parathyroidectomy, gradual resolution of metastatic calcification in the affected areas occurs. The case presented documents the consequence of secondary hyperparathyroidism with calcification of mammary vessels leading to severe breast pain with resolution of the pain and vessel calcification after renal transplantation.     

Diffuse pulmonary hemorrhage and rapidly progressive renal failure. An uncommon presentation of Wegener's granulomatosis.

A 57 year old woman presented with rapidly progressive renal failure and diffuse pulmonary hemorrhage and life-threatening respiratory failure promptly developed; these conditions resolved after bilateral nephrectomy. Renal pathology revealed rapidly progressive glomerulonephritis and vasculitis with granular deposition of immunoglobulin on immunofluorescent staining. One year later, multiple nodular cavitating pulmonary infilrates developed, and lung biopsy was diagnostic of Wegener's granulomatosis. Therapy with cyclophosphamide resulted in resolution of the pulmonary lesions. Diffuse pulmonary hemorrhage and rapidly developing renal failure mimicking Goodpasture's syndrome was the initial manifestation of Wegener's granulomatosis in this patient.