Renal Cortical Nephrocalcinosis Following Acute Renal Failure Due to Polytrauma

Renal cortical nephrocalcinosis is a rare condition in which there is calcification within the renal parenchyma. This article reports a 33-year-old patient who developed acute renal failure following multiple injuries leading to hemorrhagic shock. His renal failure improved gradually, though he required dialysis support for two months. Serial ultrasounds showed a progressive decrease in renal size, and a radiograph of the abdomen showed speckled calcification in both renal areas. A CT scan of abdomen showed diffuse cortical calcification involving the entire right kidney and upper half of the left kidney.     

Bilateral cortical necrosis and calcification of the kidneys following snakebite: a case report.

A 16 year-old-boy was admitted to the ICU of university hospital with acute renal failure following snakebite. The clinical evolution of the patient associated with radiological findings of renal calcification suggested bilateral cortical necrosis of the kidneys. The biopsy findings were compatible with this diagnosis. The patient was discharged 86 days after his admission, with chronic renal failure, since a kidney transplantation was not possible.     

A case of multilocular renal cyst with calcification

A 55-year-old woman was incidentally found to have a calcified right renal mass on ultrasonography. A plain film of the abdomen revealed a 3.5 X 4.4 cm, curvilinear calcification in the midportion of the right kidney, and an excretory urogram showed no compression or distortion of the pelvocalyceal system. Computed tomography demonstrated a low density renal mass associated with both peripheral and central calcification. Renal arteriogram revealed a hypovascular mass. Right nephrectomy was performed and the multilocular renal cyst with calcification was confirmed histologically. In the Japanese literature, 53 cases of multilocular renal cyst have been reported, but calcification of the multilocular renal cyst seems to be the first as far as we know.     

A case of renal angiomyolipoma with bone formation

A case of renal angiomyolipoma with bone formation is reported. A 61-year-old woman was admitted to our hospital with one month history of fever. About 15 cm in diameter mass was palpated in her right lower abdomen. Plain abdominal roentgenography, ultrasonography and computed tomography showed marked calcification in the cephalic portion of the right kidney, tumors surrounding right kidney and another tumor in the right lower abdomen. All these tumors and the kidney constituted a big mass continuously, and no fatty component was demonstrated. Total excision of the mass including the kidney was performed. The mass was 30 X 24 X 10 cm in size and 3,240 g in weight. Histologically, the tumor was compatible to renal angiomyolipoma. But, radiopaque shadows which looked like calcification were disclosed to be bones, and fatty tissues were not seen so much. Therefore, the name "benign mesenchymoma" was thought to be more acceptable than angiomyolipoma in this case. Preoperative diagnosis of renal angiomyolipoma is the demonstration of fatty densities in the tumor, and the characteristic extrarenal development should also be taken into consideration. Furthermore, the bone formation of angiomyolipoma, which is very rare might be an important finding to angiomyolipoma.     

Severe calcification in a horseshoe kidney. A case report.

Marked calcification in a horseshoe kidney of a Black patient in terminal renal failure is described. The role of pyelonephritis in producing the severe calcification in a horseshoe kidney is discussed. One of the complications of a horseshoe kidney is renal stone.     

Reduced renal prepro-epidermal growth factor mRNA and decreased EGF excretion in ARF

Levels of prepro epidermal growth factor (EGF) mRNA in renal cortical tissue and urinary EGF excretion have been determined during cisplatin and ischemia-induced acute renal failure in the rat. Northern analysis of polyadenylated RNAs of kidney cortical tissue showed diminished renal preproEGF mRNA in rats injected with cisplatin (5 mg/kg). The decrease in preproEGF mRNA occurred as early as 12 hours in the kidney and persisted for at least three days after cisplatin injection. The submandibular gland, a major site of EGF synthesis, contained normal levels of preproEGF mRNA. Transplatin, a non-nephrotoxic isomer of cisplatin, did not reduce renal preproEGF mRNA levels. Northern analysis of polyadenylated RNAs of kidney cortical tissue 24 hours after a 50 minute period of renal pedicle clamping also showed reduced preproEGF mRNA levels. By contrast, cisplatin increased renal c-fos mRNA. Urinary EGF excretion was also reduced after cisplatin and ischemia and the decrease in EGF excretion correlated significantly with the degree of renal failure. The data show that nephrotoxic and ischemic renal cell injury reduces preproEGF mRNA and urinary EGF excretion. Reduced preproEGF mRNA and diminished EGF excretion may be important in the functional and regenerative responses to renal injury.     

Simple cyst arising in a transplanted kidney: a case report.

A 17-year-old girl was hospitalized for evaluation of gradually decreasing function of a kidney transplanted 8 years earlier. A plain film of the abdomen showed a possible renal calculus. Excretory urography proved that this calcification was slightly anterior to the kidney but in the upper pole a well rounded mass was discovered. An echogram confirmed the diagnosis of benign renal cyst. Malignant cystic lesions obviously must be differentiated from those that are benign. Patients on immunosuppressive therapy are known to have a higher incidence of malignancy than the general population. A malignant tumor may require withdrawal of immunosuppressive therapy and removal of the transplanted organ, whereas a benign cyst would require no therapy unless it becomes infected or produces obstruction.     

Soft tissue calcification in pediatric patients with end-stage renal disease

Soft tissue calcification is a recognized complication of uremia in adult patients and has been implicated as a cause of ischemic necrosis, cardiac arrhythmias, and respiratory failure. However, soft tissue calcification has been regarded as rare in pediatric renal patients. Following a sudden death due to pulmonary calcinosis in an adolescent after renal transplantation, we retrospectively reviewed clinical, biochemical and autopsy data of 120 patients with uremia, on dialysis, or following renal transplantation cared for at Childrens Hospital of Los Angeles from 1960 to 1983. Soft tissue calcification was found in 72 of 120 patients (60 percent). Forty-three patients (36 percent) had systemic calcinosis (Group A): the most frequent sites of mineral deposition were blood vessels, lung, kidney, myocardium, coronary artery, central nervous system, and gastric mucosa. Vascular calcification was uniformly accompanied by deposits in other organs. Twenty-nine patients had small amounts of focal calcification (Group B) and 48 patients had no soft tissue calcification (Group C). By multiple logistic regression analysis, the use of vitamin D or its analogues, the form of vitamin D medication prescribed, the peak calcium x phosphorus product, the age at onset of renal failure, and male sex were jointly associated with calcinosis (Group A). Vitamin D therapy showed the strongest independent association with calcinosis and the probability of calcinosis was greater in patients receiving calcitriol when compared with dihydrotachysterol and vitamin D2 or D3. The duration of renal failure, peak serum calcium, serum calcium at death, serum phosphorus at death, and primary renal diagnosis, were not statistically associated with calcinosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Aggressive Pulmonary Calcification Developed After Living Donor Kidney Transplantation in a Patient With Primary Hyperparathyroidism

Metastatic pulmonary calcification, defined as calcium deposition in the intact lung, is commonly seen in patients with chronic renal failure, and it is known to be a benign clinical condition when detected by chance in an asymptomatic patient. Here we report the case of a 33-year-old woman who developed rapid and aggressive metastatic pulmonary calcification shortly after a living donor kidney transplantation, which induced acute antibody-mediated rejection. The patient's metastatic pulmonary calcification was successfully improved by extensive treatment for graft rejection, the correction of her accompanying primary hyperparathyroidism, and medical treatment with a bisphosphonate and sodium thiosulfate. Aggressive pulmonary calcification is reported as a rare complication seen in patients who have undergone a failed renal transplantation. A failed renal graft and accompanying secondary hyperparathyroidism seem to accelerate metastatic calcification. Most of the patients who develop aggressive pulmonary calcification suffer from the rapid progression of dyspnea and occasionally fever, and they die of respiratory failure. Pulmonary calcification should be considered in a patient developing dyspnea and unexplained pulmonary infiltrate, especially in the context of renal graft rejection; otherwise the prognosis of the patient will be very poor.     

Cortical benign fibromatous tumor (fibroma) of the kidney.

Benign fibromatous tumor (BFT), also named 'fibroma', is a distinctive clinico-pathologic entity occurring in epididymis, spermatic cord, paratesticular structures, testis, renal peripelvis and rarely in renal parenchyma. We report the first case of a BFT (fibroma) located in the cortex of the kidney, and a critical review on the topic is provided. Tumor was found incidentally at autopsy as a small cortical nodule. With the increasing use of radiological imaging of the abdomen, it is likely that an increased number of incidental and asymptomatic benign renal tumors will be diagnosed. We underline that BFT (fibroma) should be considered in the preoperative differential diagnosis of renal cortical nodules.     

Renal cortical uptake kinetics of gentamicin in rats with impaired renal function

The renal cortical uptake kinetics of the aminoglycoside antibiotic gentamicin was determined in the remnant kidney model. Renal failure was induced by partial ablation of the right kidney followed by left nephrectomy in female Wistar rats. The animals received a six-hour gentamicin infusion at a constant rate yielding steady-state serum concentrations ranging from 0.5 to 150 micrograms/mL. The renal cortical gentamicin concentrations were determined and related to the serum concentrations achieved. This relationship was nonlinear and followed Michaelis-Menten kinetics. Gentamicin cortical uptake rate, however, did not show clear saturation in the range of gentamicin serum levels studied as was observed in rats with normal renal function. The Michaelis-Menten parameters determined by nonlinear regression were Km = 15.0, 73.9, and 135.7 micrograms/mL; and Vmax = 149.9, 213.7, and 239.2 micrograms/g cortex/h, respectively, for controls, rats with serum creatinine levels between 0.9 and 1.2 mg/dL, and those with levels between 1.3 and 1.8 mg/dL. It is concluded that at serum levels below 100 micrograms/mL, the gentamicin renal cortical uptake is diminished in rats with renal failure. This decrease in renal cortical uptake is more pronounced in the group of rats with more severe renal failure.     

Imaging of infantile polycystic kidney disease with some rare association.

Seventeen patients, age 1 day to 6 years with infantile polycystic kidney disease were evaluated with ultrasound and other imaging techniques. Most patients showed bilaterally enlarged kidneys with hyperechoic renal parenchyma, which had poor differentiation in outlines as well as between renal sinus, cortex and medulla. Cysts of various sizes were also identified in the kidneys. However, a third of these cases showed well-defined renal outlines, normal echogenic cortical rim, whilst dilated renal collecting systems were seen in another third of the cases. Twelve cases showed hepatomegaly. Few rare findings such as liver cysts, associated Meckel syndrome, renal stone, bilateral vesicoureteric reflux and renal calcification were also noted. This study confirms the diagnostic value of sonography and intravenous pyelography examination. However, the noninvasiveness and the opportunity for repeat examination in antenatal and postnatal life makes sonography the ideal investigative modality.     

Reninoma treated with nephron-sparing surgery

A 14-year-old hypertensive boy was evaluated in our clinic. The physical examination was essentially normal except for his high blood pressure. Laboratory findings showed increased plasma renin activity. Abdominal ultrasonography detected a hypoechoic, 2-cm mass in right kidney. Contrast-enhanced computed tomography of the abdomen revealed a well-circumscribed, solid, hypoenhancing cortical lesion in the middle of the right kidney. Magnetic resonance angiography documented bilateral normal renal arteries. With a preoperative diagnosis of reninoma, the patient underwent nephron-sparing surgery. Intraoperative frozen section analysis revealed a benign lesion. Subsequently, histopathologic examination and electron microscopy confirmed the diagnosis of juxtaglomerular cell tumor. The patient remained normotensive in the postoperative period. Follow-up intravenous urography showed bilateral normally functioning kidneys.     

Preservation of normal cortical vasculature in ischaemic renal failure in the dog.

Ischaemic renal failure in the dog was studied by clamping one renal artery for 2 hr in 18 animals. Total renal blood flow was measured for 3 hr after this and only reduced by about 30%. Fine detail renal angiography showed a normal cortical perfusion pattern. Urine flow rates and creatinine clearances from these kidneys, however, were found to be grossly impaired over this period. Seven days later the angiogram of the oliguric kidney remained normal. Two-hour unilateral renal ischaemia in the dog leads to a form of acute renal failure with a striking disparity between glomerular perfusion and clearance, arguing agains a primary circulatory defect.     

The influence of dietary calcium on kidney calcification and renal function in rats fed high-phosphate diets

This study was carried out to test the hypothesis that kidney calcification caused by high dietary phosphorus intake can be prevented by increasing the calcium content of the diet, because the latter reduces the intestinal P absorption. The investigation was conducted in rats fed semipurified diets with either a low (0.15%) or a high (1.20%) P content. Although dietary Ca supplementation (as CaCO3 or CaCl2) reduced the intestinal P absorption, it did not prevent kidney calcification induced by high dietary P. On the contrary, when CaCO3 was supplemented for 16 weeks, renal calcification increased, probably due to the alkaline nature of this salt. Both CaCO3 and CaCl2 in the high-P diets adversely influenced Mg use. This might explain the failure of these salts to prevent kidney calcification.     

A Comparison of Calcium to Zoledronic Acid for Improvement of Cortical Bone in an Animal Model of CKD

Patients with chronic kidney disease (CKD) have increased risk of fractures, yet the optimal treatment is unknown. In secondary analyses of large randomized trials, bisphosphonates have been shown to improve bone mineral density and reduce fractures. However, bisphosphonates are currently not recommended in patients with advanced kidney disease due to concern about oversuppressing bone remodeling, which may increase the risk of developing arterial calcification. In the present study we used a naturally occurring rat model of CKD with secondary hyperparathyroidism, the Cy/+ rat, and compared the efficacy of treatment with zoledronic acid, calcium given in water to simulate a phosphate binder, and the combination of calcium and zoledronic acid. Animals were treated beginning at 25 weeks of age (approximately 30% of normal renal function) and followed for 10 weeks. The results demonstrate that both zoledronic acid and calcium improved bone volume by micro–computed tomography (µCT) and both equally suppressed the mineral apposition rate, bone formation rate, and mineralizing surface of trabecular bone. In contrast, only calcium treatment with or without zoledronic acid improved cortical porosity and cortical biomechanical properties (ultimate load and stiffness) and lowered parathyroid hormone (PTH). However, only calcium treatment led to the adverse effects of increased arterial calcification and fibroblast growth factor 23 (FGF23). These results suggest zoledronic acid may improve trabecular bone volume in CKD in the presence of secondary hyperparathyroidism, but does not benefit extraskeletal calcification or cortical biomechanical properties. Calcium effectively reduces PTH and benefits both cortical and trabecular bone yet increases the degree of extra skeletal calcification. © 2014 American Society for Bone and Mineral Research.     

Vascular calcification: contribution of parathyroid hormone in renal failure

Hyperphosphatemia is a driving force in the pathogenesis of vascular calcification (VC) and secondary hyperparathyroidism associated with renal failure. To test for the possible contribution of parathyroid hormone (PTH) to cardiovascular calcification, we removed the parathyroid glands from rats but infused synthetic hormone at a supraphysiologic rate. All rats were pair-fed low, normal, or high phosphorus diets and subjected to a sham or 5/6 nephrectomy (remnant kidney). Control rats were given a normal diet and underwent both sham parathyroidectomy and 5/6 nephrectomy. Heart weight/body weight ratios and serum creatinine levels were higher in remnant kidney rats than in the sham-operated rats. Remnant kidney rats on the high phosphorus diet and PTH replacement developed hyperphosphatemia and hypocalcemia along with low bone trabecular volume. Remnant kidney rats on the low phosphorus diet or intact kidney rats on a normal phosphorus diet, each with hormone replacement, developed hypercalcemia. All rats on PTH replacement developed intense aortic medial calcification, and some animals presented coronary calcification. We suggest that high PTH levels induce high bone turnover and medial calcification resembling M?mckeberg's sclerosis independent of uremia. This model may be useful in defining mechanisms underlying VC.     

Protective effect of prostaglandin E1 on ischemia-induced acute renal failure in dogs

The protective effect of intravenous administration of exogenous prostaglandin E1 on ischemia-induced acute renal failure was investigated in dogs. The parameters studied were renal cortical blood flow, renal function, survival time, and histologic changes. The model was prepared by clamping the renal artery for 1 or 2 hours. Renal cortical blood flow was measured by the hydrogen washout technique. After prostaglandin E1 administration, renal cortical blood flow increased significantly and renal function was maintained at relatively high levels with low serum creatinine and moderate creatinine clearance levels. Mean survival time increased markedly from 4.1 to 35.2 days by administration of prostaglandin E1. Ischemia-induced acute renal failure is usually accompanied by zonal necrosis of renal tubules prominent in the cortex. However, occurrence of these histologic damages could be virtually prevented by prostaglandin E1 administration (i.e., only minimal tubular necrosis was found in a small area of the cortex). We conclude from this study that postischemic administration of exogenous prostaglandin E1 does provide a certain degree of protection for the kidney, which may have a great clinical implication in improving the success rate of kidney transplantation, especially of cadaver donor kidneys.     

A case report of extensively calcified renal cell carcinoma

A 73-year-old woman visited another hospital with complaints of occasional episodes of gross hematuria. A computed tomographic (CT) scan revealed extensive calcification in the left kidney, and she was referred to our hospital for further examinations. The physical examination was unremarkable other than mild back pain on her left side. Blood chemistry was normal. The CT scan revealed a mildly enhanced tumor of 6 cm in diameter accompanied by extensive calcification in the left kidney. Angiography revealed a hypovascular tumor in the left kidney. A left radical nephrectomy was carried out. Gross appearance of the specimen showed extensive calcification from the renal pelvic to the parenchyma of the lower pole of the left kidney. The histopathological diagnosis was renal cell carcinoma, alveolar type, mixed subtype, pT2pN0pM0.     

Advanced abdominal arterial calcification sparing kidney allograft—case report

Abstract

Excess and progressing arterial calcification is a frequent finding in patients with chronic kidney disease and in diabetics. Vascular calcification present in patients on dialysis, usually continues to progress (although possibly with slower rate) in patients after kidney transplantation. These observations are limited mostly to aorta and coronary arteries; virtually no data exist on progression in vascular calcification within the vasculature of transplanted kidney. The case report presents the patient with diabetes and non-functioning renal transplant back on dialysis with extremely severe intra-abdominal artery calcification, sparing renal artery of transplanted kidney. Calcification did not develop within transplanted kidney despite 10 years of exposition to diabetic environment and a few years of chronic kidney disease after transplantation, including CKD-T stage 5 for at least one year after re-starting of dialysis. To the best of our knowledge, this is the second report ever describing sparing of kidney graft from calcification despite disseminated calcification in other vascular beds. It is tempting to speculate that some “intrinsic” factors exist within the transplanted kidney that protects it from calcification despite exposure to procalcifying milieu of diabetes and uremia.