Necrosis papilar renal bilateral de resolución espontánea como causa de hematuria microscópica. Caso clínico / Bilateral renal papillary necrosis of spontaneous resolution as a cause of microscopic hematuria. Report of one case

Renal papillary necrosis is an infrequent cause of hematuria characterized by ischemic necrosis of the renal medulla, especially the papilla. Its most common cause is analgesic abuse. Despite being oligo-symptomatic, in many cases its presence is associated with serious functional sequelae. Imaging, especially computed tomography, is essential to make the diagnosis. We report a 63-year-old female studied for an asymptomatic microscopic hematuria whose tomographic study showed a bilateral renal papillary necrosis. No etiology was found, and she evolved with a spontaneous complete remission.

Necrosis papilar renal: el diagnóstico de un clásico en la era de la tomografía multidetector / Renal papillary necrosis: the diagnosis of a classic in the era of the multislice computed tomography

La necrosis papilar renal es una condición originada por múltiples factores, con consecuencias variadas incluyendo dentro de ellas el desarrollo de insuficiencia renal terminal y eventualmente la muerte. Su presentación en la pielografía de eliminación demuestra múltiples patrones de excavación papilar, que están muy bien descritos en la literatura clásica. Con el advenimiento de la urografía por tomografía computada multicorte, estos hallazgos han sido refinados, agregándose también nuevos signos, que incluyen, entre otros, la detección de cambios medulares precoces que podrían implicar, en un futuro cercano, un significativo cambio en la evolución y pronóstico de estos pacientes. En esta publicación hacemos una revisión y puesta al día de los aspectos imaginológicos de la necrosis papilar renal.

Renal papillary necrosis is a multifactorial entitiy that encompasses a wide range of consecuences, including end-stage renal impairment or even death. Its appearance on intravenous pyelography pictures reveals multiple patterns of papillary excavation, fairly well defined in traditional literature. With the advent of multislice computed tomography urography these findings have been refined and new radiological signs such as detection of early renal medullary changes, among others, have been added. The application of this imaging modality may translate into significant short-term improvements in the evolution and prognosis of these patients. This paper is intended to provide both a reviewing and an updating of renal papillary necrosis imaging issues.

Indinavir-associated toxicity mimicking urinary tuberculosis in a patient with AIDS

This case reported to a patient with AIDS who presented persistent sterile leukocyturia and hematuria, lower back pain, bladder suffering symptoms, and renal papillary necrosis which were thought to be secondary to urinary tuberculosis but were demonstrated to be indinavir-associated side effects. The intention of this report is to remind medical professionals involved in the care of HIV+ patients of this possible association in order to avoid unnecessary investigation and to stress the need of careful periodical assessment of renal function and urinalysis in patients treated with indinavir.

A Case of Analgesic Nephropathy Complicated by Transitional Cell Carcinoma of the Ureter / 대한신장학회잡지

Following a report by Hultengren et al. (Acta Chir Scand, 1965), it has been suggested that analgesic abuse predisposes to urothelial neoplasia. Urinary tract malignancy is combined in 8-10% of patients with analgesic nephropathy. Microscopic or gross hematuria can be the first sign leading to the diagnosis of uroepithelial malignanacy in analgesic abusers. Since uroepithelial malignancies found in analgesic abusers tend to be multiple and have a worse prognosis, continued monitoring is essential, and new hematuria should be evaluated with urinary cytology, and cystoscopy with reterograde pyelography. Phenacetin found to be the chief cause of malignancies in analgesic abusers, it has been anticipated to be a human carcinogen and was banned as an OTC drug since 1987. But still there remains a debate whether acetaminophen and other compound analgesic components are carcinogenic. We report the case of a 58-year-old man with a history of analgesic abuse who was diagnosed with transitional cell carcinoma combined with analgesic nephropathy. We also review the literature.

Candidal REnal Papillary Necrosis Treated with Bilateral Nepherectomy: Report of a Case / 대한신장학회잡지

Renal papillary necrosis(RPN) is a 4bointerstitial nephropathy accompanied by compromised medullary blood flow that ultimately results in a focal or diffuse ischemic necrosis of segments of the renal medulla. Renal papillary necrosis is infrequently reported as complication of fungal infections. Underlying condi- tions such as prematurity, immunosuppressive therapy, neoplastic disease, previous antibiotic therapy, diabetes mellitus, extensive burn and indwelling vascular catheters were found in candidal RPN. Candidal renal papillary necrosis is a extremely rare and fatal disease. Only 20 cases were reported over the past. There were only three survivors which were diagnosed were treated with antifugal agents early in the clinical course. As far as we know, this case is the first case of candidal RPN treated with bilateral nephrectomy. We report a case of candidal renal papillary necrosis in a 66-year-old diabetic woman treated with bilateral nephrectomy, along with review of the literatures.

A Case of Renal Papillary Necrosis Associated with Diabetes Mellitus / 대한비뇨기과학회지

Renal papillary necrosis is rare. It usually occurs in association with diabetes mellitus, pyelonephritis, urinary tract obstruction, analgesic abuse and sickle cell hemoglobinopathies. The basic pathophysiologic process in renal papillary necrosis appears to be ischemic necrosis. We experienced a case of renal papillary necrosis associated with diabetes mellitus. This 59 years old female was diabetic for 10 years and had persistent pyuria, not controlled with antibiotics. The excretory urography showed nonvisualized left kidney and retrograde pyelography showed multiple irregular filling defect in pelvis and ureter. The nephrectomized kidney showed typical findings of papillary necrosis, grossly and microscopically.

A Study on the Pathogenesis of Renal Papillary Necrosis Induced by Endotoxin

The author carried out an experimentation to clarify a possible pathogenesis of renal papillary necrosis induced by an univisceral Shwartzman reaction. The experimental animals were healthy white rabbits in weighing between 1.7 kg and 3.0 kg. Under the condition of ureterostomy, animals were pretreated with 0.5 cc of 50% ethyl alcohol and followed by administration of 0.2 ~ 1.5 mg endotoxin (E. coli 026 : B6, bacto lipopolysaccharide B. Difco, U.S.A.) as preparation in the renal pelvis. And then sacrificed at 10 minutes, 30 minutes, 1 hour, 2 hours, 6 hours and 24 hours after intravenous injection of 0.2 mg or 0.6 mg endotoxin through the ear veins, subjection to examine light and electron microscopically. The obtained results were summarized as follows: Papillary necrosis was developed in 88% among 18 cases excluding 6 cases died before sacrification. There were two types of necrosis, namely papillary and medullary type, but the former and combined forms of both types were the most common findings. Initial main target site of injury in renal papilla induced by endotoxiin was the endothelium of vasa recta and then followed by the Henle's loop, interstitial cell and collecting tubule respectively. Vascular injuries such as swelling and detachment of endothelium were observed since 10 minutes after endotoxin injection. Henle's loop showed stratification of basement membrane without consistent features with time lapses and initially observed fatty vaculoes at 1 hour after endotoxin injection were more eminent in 24 hours group. Main changes of interstitial cells were decrease of lipid droplets while increase of fatty vacuoles; the latter were initially observed in 1 hour group and more eminent in 24 hours group. Collecting tubule showed many fatty vacuoles especially in 24 hours group. It is thought that emergence of fatty vacuoles seems to be a kind of immature lipid droplets to compensate the increased demand of PC release due to continuous ischemic condition. In conclusion, it is thought that ischemic injury due to the vascular changes is pathogenic mechanism producing renal papillary necrosis. Endotoxin induced univisceral Shwartzman reaction in the kidney may be a good experimental model in studying renal papillary necrosis.

An Experimental Study on Effects of Renal Papillectomy and Partial Ureteral Ligation on the Kidney / 대한비뇨기과학회지

Necrosis of the papilla and chronic interstitial nephritis of the renal cortex are the two renal 1esions most commonly. described in cases of analgesic nephropathy. Some authors believed that the necrosis of the papilla was secondary to the cortical changes by which fibrosis of the cortex produced ischemia of papilla and necrosis. However, other authors have suggested that the pathogenesis is, in fact, the reverse and that the cortical changes in analgesic nephropathy are caused by the medullary necrosis. An experimental study was therefore undertaken to clarify this problem and also to determine the influence of increased intrapelvic pressure on the postpapillectomy renal alterations. Followings are the results: 1. In 'the group having renal papillectomy, marked tubular dilatation and interstitial edema of the medulla are prominent changes upto two weeks after removal of the papilla. Tubules are usu. ally filled with various casts. After three weeks, there starts the tubular atrophy and interstitial fibrosis with mil infiltration of inflammatory cells. The tubular atrophy and renal scarring become much severe and diffuse six weeks after papillectomy. but glomeruli remain relatively intact. 2. The degree of tubular changes and parenchymal scarring are assumed influential to the size of removed papilla. The tubular atrophy is prominent in distal convoluted tubules and collecting tubules, and the interstitial changes extend from the medulla to the cortex in the late stage. 3. Focal or scattered depositions of amorphous calcium or calcium oxalate are found in about one fourth of cases. 4. In the group having partial ureteral ligation a week after renal papillectomy, the tubular and interstitial changes appear earlier and are more remarkable than those of papillectomy alone. The inflammatory reaction is also more prominent, and conglomeration of glomerulus is noted in some instances of the later stage. The form of the renal scarring found in this experimental study closely resembles that seen in analgesic nephropathy in man. This findings support the view that the cortical lesions in analgesic nephropathy develop as a direct consequence of papillary necrosis and additional ureteral ligation enhances interstitial nephritic process. It is possible that the tubular atrophy and interstitial edema that develop shortly after removal of the papilla may produce cortical changes.

Renal Papillary Necrosis / 대한비뇨기과학회지

Diabetes mellitus, obstructive uropathy and urinary infection were considered to be most important in the etiology of renal papillary necrosis in the past literature. However, since 1953, Spuhler and Zollinger reported an association between phenacetin abuse and renal papillary necrosis, the most frequent cause of renal papillary necrosis has been diabetes mellitus, while analgesic abuse (contained phenacetin) has been the second most common factor in recent reports. In the more recent literature, most of the patient have had neither obstructive uropathy nor urinary infection, and it is quite possible that there two condition are of no direct etiological significance. But in this case, we can not suggest definite etiological factor except urinary infection clinically. Only one case is reported showing clinical manifestations laboratory findings, pyelographic findings and pathological changes compare with previous papers.