Episodes Of Gross Hematuria Research Articles

A phase I clinical trial of 12- O-tetradecanoylphorbol-13-acetate for patients with relapsed/refractory malignancies

Phorbol esters activate protein kinase C and modulate a variety of downstream cell signaling pathways. 12-O-tetradecanoylphorbol-13-acetate (TPA) is a phorbol ester that induces differentiation or apoptosis in a variety of cell lines at low concentrations. A phase I dose escalation trial of TPA was undertaken for patients with relapsed or refractory malignancies. The starting dose was 0.063 mg/m2 and most patients were treated with an intravenous infusion of TPA on days 1-5 and 8-12 followed by a 2-week rest period prior to retreatment. Thirty-five patients were treated. A biological assay was used to monitor levels of TPA-like activity in the blood after treatment. Serious adverse events included individual episodes of gross hematuria, a grand mal seizure, syncope, and hypotension. Many patients had transient fatigue, mild dyspnea, fever, rigors, and muscular aches shortly after the infusion. Dose-limiting toxicities included syncope and hypotension at a dose of 0.188 mg/m2. Only a single patient had evidence of tumor response. These studies establish 0.125 mg/m2 as the maximally tolerated dose when TPA is administered on this schedule.

Malignant Paraganglioma of the Urinary Bladder: Immunohistochemical Study of Prognostic Indicators

Using various immunohistochemical markers, the objective of our study was to assess whether correlation exists between growth potential of paraganglioma (pheochromocytoma) cells and formation of metastasis. The patient was a 28-yr-old man who presented with intermittent episodes of gross hematuria due to a mass in the urinary bladder. He had no constitutional symptoms to suggest paraganglioma. Histologic, immunohistochemical, and electron microscopic investigation of the surgically removed tissue proved that the tumor was a malignant paraganglioma with metastases in the regional lymph nodes. The immunohistochemical tests were not supportive of high cell proliferation index, indicating that metastases can develop in the absence of rapid multiplication of the tumor cells. Abnormalities in vascular architecture and marked expression of VEGF in the tumor cells may be regarded as prognostic signs to predict the formation of metastases.

Involvement of tonsils in IgA nephropathy

This study was intended to clarify the involvement of tonsils in the pathogenesis of IgA nephropathy. In 62 patients with IgA nephropathy and 20 patients with other renal diseases, their tonsils were stimulated by an ultra short wave. Forty of 62 patients with IgA nephropathy (65%) showed a deterioration of urinary findings after the stimulation compared with six of 20 patients with other renal diseases (30%). Previous episodes of gross hematuria following upper respiratory tract infections existed in 17 of 40 patients (Group A) who showed a deterioration of urinary findings after tonsil stimulation (43%) as against in four of 22 (Group B) without the deterioration (18%). The level of serum secretory IgA was higher in Group A than in Group B. It is suggested that chronic tonsillitis may play an important role in the development of IgA nephropathy. Thirty-six patients received tonsillectomy from 1980–2002. The frequency of gross hematuria at upper respiratory infection decreased in 56% of the patients. The amount of urinary protein decreased in 33% of the patients and RBC counts decreased in 56% of the patients. Eight patients with tonsillectomy were followed up longer than 16 years. Two of them went to hemodialysis and five of them showed no urinary abnormalities at present. The effect of tonsillectomy in the long term was not clarified in this study.

Is Cytology Required for a Hematuria Evaluation?

The value of urine cytology in evaluating patients with hematuria remains controversial. The American Urological Association Best Practice Policy on Asymptomatic Microscopic Hematuria recommends cytology only in patients with risk factors for transitional cell carcinoma (TCC). This study evaluated how often urine cytology yielded supportive or unique information that led to the diagnosis of transitional cell carcinoma, the cost of that information and whether it would have been obtained using the current best practice policy. Between March 1976 and June 1985, 1,000 sequential patients with 1 episode of gross hematuria or microscopic hematuria, defined as greater than 3 red blood cells per high power field on 2 of 3 properly collected urinalyses, were evaluated according to a standard protocol in a closed panel health care system in the state of Hawaii. These records were reviewed to determine if urine cytology yielded supportive or unique information that led to the diagnosis of TCC. In 4 patients positive urine cytology was the sole finding supporting a TCC diagnosis. Urine cytology had a sensitivity of 55% and a specificity of 99.3%. The cost of a cytology result that yielded unique information was 8,367 US dollars using the 2002 Medicare reimbursement schedule. Urine cytology can have an important role in the evaluation of hematuria. The current American Urological Society Best Practice Policy using risk factors to select patients for urine cytology would have captured the 4 patients for whom cytology was the key to diagnosis. Urine cytology was comparable to excretory urography, creatinine and cystoscopy in terms of cost analysis.

The Proteus Syndrome Associated With Life Threatening Hematuria

The Proteus syndrome (PS) is a recently defined rare hamartomatous disorder. 1 PS comprises an association of verrucous epidermal nevi, infantile hemangiomas, lipomalike subcutaneous hamartomas and asymmetrical overgrowth of almost any part of the body. Vascular anomalies of the gastrointestinal tract, spleen, kidneys and testicles have been reported. To our knowledge we report the first case of bladder involvement in PS. CASE REPORT A 2-year-old girl was admitted to the hospital for treatment of extensive verrucous nevi and large hemangiomas involving mainly the right hemibody. The lesions also involved the right mandibular and periorbital area. The cutaneous lesions had been present since birth and were progressively increasing. She had multiple recent episodes of gross hematuria. The only laboratory abnormality was microscopic hematuria. The gross hematuria episodes prompted complementary evaluation of the urinary tract and adjacent organs. Thoracic, abdominal and pelvic computerized tomography revealed extensive vascular (venous) lesions involving the right lung, right medulla and right hemipelvis overlying a thickened and irregular bladder. The kidneys and ureters were normal. Voiding cystogram confirmed the irregular and nodular aspect of the right hemibladder wall (fig. 1). At cystoscopy extensive venous lesions involving the right hemibladder (excluding the trigone) were seen (fig. 2). Within a few days the child returned with acute massive gross hematuria with clot. A pre-shock state (hemoglobin 38) led to immediate intervention with a combination of selective bilateral internal iliac artery branch embolizations, cystoscopic declotting and bladder irrigation, which achieved control of the bladder hemorrhage. Because this child lived in a remote area, we had to consider a more definitive treatment. We opted for an endoscopic approach using a potassium titanium phosphate laser. At the time of surgery balloon catheters were placed in the internal iliac arteries in case of massive bleeding and conversion to open surgery. The venous lesions were treated in a sweeping fashion using 193 J total energy. At 3-year followup gross hematuria had not recurred and the child was thriving well. Control cystoscopy revealed an important but incomplete regression of the venous lesions. DISCUSSION To our knowledge the association of extensive intravesical venous lesions and PS has not been reported previously, and was a therapeutic challenge. An open approach (partial cystectomy) was entertained. However, the extent of the pelvic vascular anomalies seen on computerized tomography and arteriogram with the risk of major hemorrhage leading to total cystectomy and ileal conduit led us to opt for a more conservative endoscopic approach. Endoscopic treatment of bladder vascular lesions (hemangiomas) is well recognized. Smith reported the use of neodymium:YAG laser coagulation in bladder hemangiomas associated with the Klippel-Trenaunay syndrome (a syndrome related to PS). 2 We chose potassium titanium phosphate laser because of its excellent coagulation capabilities and superficial tissue penetration. 3 Despite the favorable out

Vesical hemangioma in patient with Klippel-Trenaunay-Weber syndrome

Klippel-Trenaunay-Weber syndrome is characterized by cutaneous hemangiomas, varicosity and bony hypertrophy of extremities. Urinary tract hemangiomas may occur in 3 to 6% of these patients. This work intends to report a case of a patient with a huge vesical hemangioma, who presented this syndrome. A 5 year-old boy with Klippel syndrome sought our services due to 3 episodes of gross hematuria in the past 30 days. Excretory urography and computerized tomography were performed, indicating the presence of a swelling in vesical dome. An exploratory cystotomy was conducted and the dark colored mass in vesical dome was excised by partial cystectomy. The histopathologic finding confirmed that it was a vesical hemangioma. Though rare, urinary tract hemangiomas must always be considered in patients with Klippel-Trenaunay syndrome.

Gross hematuria after prostate brachytherapy

Objectives To summarize the clinical course of postimplant gross hematuria occurring past the perioperative period. Methods From 1998 to 2000, 226 patients were treated for prostate carcinoma by implant alone or implant with supplemental external beam radiotherapy, using palladium-103 or iodine-125. Of these 226 patients, 9 had incomplete follow-up information and 2 died of causes other than prostate cancer. As a part of their routine follow-up, the remaining 215 patients were regularly mailed self-reporting questionnaires regarding urinary incontinence and hematuria. Postimplant computed tomography-based dosimetry was available for 211 (98%) of 215 patients. Dosimetric parameters were recorded for each patient using standardized methods. The rates of hematuria resolution were calculated using the product-limit (Kaplan-Meier) method. Statistical significance was determined using unpaired t testing. Results Twenty-seven patients (13%) reported at least one episode of gross hematuria occurring more than 1 week after prostate implantation. The onset and duration of bleeding varied widely. Eleven patients reported only a single, isolated episode, and 16 patients reported multiple episodes, ranging from isolated sporadic to multiple times per day. No patient required a blood transfusion. The median time from the first episode of hematuria to resolution was 3 months. Of the 27 patients who reported hematuria, 88% had resolved by 24 months from time of first bleeding. Hematuria was unrelated to the maximal or mean urethral dose. Conclusions Gross hematuria after brachytherapy resolves spontaneously in nearly all patients. Nonetheless, in patients without a recent workup for a genitourinary malignancy other than prostate cancer, a hematuria workup is reasonable. Because of the retrospective nature of this study and the highly variable presentation and clinical course of postimplant gross hematuria, we are unable to make firmer conclusions or recommendations regarding the role of follow-up urinalysis, urine cytology, anticoagulant medication, or supplemental beam radiation. Such an analysis will require a more controlled, prospective study of a large implant patient population.

Hématurie macroscopique révélant une drépanocytose hétérozygote : à propos de dix observations

Purpose. – Though currently asymptomatic, a sickle cell trait can be responsible for renal abnormalities with macroscopic hematuria. Methods. – Ten patients were admitted to our department with gross hematuria in sickle trait. Results. – Six blacks men and four blacks women, aged from 17 to 53 years, had recurrent episodes of gross hematuria with clots in five patients and lumbar pain in four patients. Duration of gross hematuria varied from two weeks to two years. Imaging findings were normal. Urinary concentration ability was abnormally low in all patients but none had an impairement of the ability to dilute the urine or tubular dysfunction. Resolution of hematuria was obtained by abundant and alkaline hydratation in three patients. In six patients, aminocaproic acid was successfully employed, with a complete (3/6) or partial (3/6) efficiency. In one last patient, oral urea permitted a partial improvement. Conclusion. – Combination of chemical and physical factors in renal medullary of sickle cell trait are reponsible for gross hematuria and impaired capacity to concentrate the urine. A cautious care must still be given to make this association a diagnostic of exclusion. Clinical is usually benign. When resting and alkaline hydration are not sufficient to resolve hematuria, antifibrinolytic agents such as aprotinin, oral urea, urologic technical are sometimes necessary.

IgA nephropathy, the most common cause of glomerulonephritis, is linked to 6q22-23.

End-stage renal disease (ESRD) is a major public health problem, affecting 1 in 1,000 individuals and with an annual death rate of 20% despite dialysis treatment. IgA nephropathy (IgAN) is the most common form of glomerulonephritis, a principal cause of ESRD worldwide; it affects up to 1.3% of the population and its pathogenesis is unknown. Kidneys of people with IgAN show deposits of IgA-containing immune complexes with proliferation of the glomerular mesangium (Fig. 1). Typical clinical features include onset before age 40 with haematuria and proteinuria (blood and protein in the urine), and episodes of gross haematuria following mucosal infections are common; 30% of patients develop progressive renal failure. Although not generally considered a hereditary disease, striking ethnic variation in prevalence and familial clustering, along with subclinical renal abnormalities among relatives of IgAN cases, have suggested a heretofore undefined genetic component. By genome-wide analysis of linkage in 30 multiplex IgAN kindreds, we demonstrate linkage of IgAN to 6q22-23 under a dominant model of transmission with incomplete penetrance, with a lod score of 5.6 and 60% of kindreds linked. These findings for the first time indicate the existence of a locus with large effect on development of IgAN and identify the chromosomal location of this disease gene.

ORTHOTOPIC RENAL TRANSPLANTATION IN A PATIENT WITH A MASSIVE PELVIC ARTERIOVENOUS MALFORMATION

Heterotopic renal transplantation is commonly performed with a high success rate. Because of the shortage of organ donors, a variety of surgical techniques exist to use organs that may have otherwise been discarded. Furthermore, a greater number of high risk patients are undergoing renal transplantation, necessitating modification of the routine heterotopic procedure.1 CASE REPORT A 32-year-old man presented for renal transplant assessment with renal insufficiency and well controlled hypertension. At 20 years old he was diagnosed with IgA nephropathy following an episode of gross hematuria and significant hypertension. Before transplantation computerized tomography revealed multiple hemangiomas throughout the right retroperitoneal space and pelvis, causing displacement of the inferior vena cava and right kidney, and compressing the bladder to the left pelvic wall (fig. 1). Malignancy was ruled out. Magnetic resonance imaging showed bilateral intermuscular, intramuscular and subcutaneous malformations in the abdomen, pelvis and groin of arterial, venous and lymphangiomatous origin (fig. 2). Cystoscopy and retrograde pyelography revealed a severely compressed bladder but a normal left ureter. Angiography demonstrated splenic and renal arteries suitable for orthotopic transplantation. Multiple areas of arteriovenous malformations were encountered intraoperatively along the flank, involving the abdominal wall and retroperitoneum. Extensive adhesions made mobilization of the recipient pathological kidney difficult. The renal vein and artery were occluded proximally, and nephrectomy was completed. The renal artery was deemed adequate for orthotopic transplantation intraoperatively. End-to-end renal artery and renal vein anastomoses were performed using 5-zero polypropylene sutures. On completion of the anastomoses (40 minutes) the kidney immediately had good color and turgor. A Hynes-Anderson pyeloplasty was completed over a 7Fr stent using running 4-zero polyglactin sutures. After insertion of a Jackson-Pratt drain, bleeding occurred from intercostal vessels and multiple retropubic hemangiomas. Blood loss was 3,000 cc, and urine output was immediate and excellent. Postoperative course was complicated by incisional bleeding which was successfully managed with packing. At the time of hospital discharge creatinine was stable at 1.6 mg./dl. (normal 0.6 to 1.3). At 1-year followup creatinine was 1.3 mg./dl., and the patient was otherwise well with no episodes of rejection. Followup ultrasound demonstrated no evidence of hydronephrosis. DISCUSSION

76-Year-Old Man With Retroperitoneal Bleeding After Prostatectomy

76-Year-Old Man With Retroperitoneal Bleeding After Prostatectomy

Familial microscopic hematuria caused by hypercalciuria and hyperuricosuria

We report 12 patients belonging to five different families in whom persistent isolated microhematuria was associated with hypercalciuria and/or hyperuricosuria. Four patients had episodes of gross hematuria, three patients had passed renal stones, and a history of nephrolithiasis was obtained in four of the families (80%). Calcium oxalate and uric acid crystals were commonly observed in the urine sediments. Urinary erythrocytes had a normal appearance on phase-microscopic examination. Reduction of calciuria and uricosuria by thiazide diuretics, allopurinol, forced fluid intake, and dietetic measures led to a persistent normalization of urine sediment with complete disappearance of hematuria. Determination of calcium and uric acid urinary excretions should be included in the study of familial hematuria.

Identification of patients with autosomal dominant polycystic kidney disease at highest risk for end-stage renal disease.

To identify those potential factors that, early in the course of disease, mark a population of patients with autosomal dominant polycystic kidney disease (ADPKD) who have worse renal survival, survival analysis and risk ratio calculation for 1215 ADPKD patients were performed. Survival times were calculated as time to dialysis, transplantation, or death. Risk ratios were calculated using the Cox proportional hazards model. Three hundred eighty-eight patients entered end-stage renal disease and 205 patients died. ADPKD2 subjects had longer renal survival than ADPKD1 subjects (median survival, 68 versus 53 yr; P < 0.0005; risk ratio, 2.5). Women had significantly better renal survival than men (56 versus 52 yr; P < 0.0001; risk ratio, 1.6). Subjects who were diagnosed before age 30 and those who developed hypertension before age 35 had worse renal survival than those subjects who were diagnosed after age 30 or those who remained normotensive after age 35, respectively (age of diagnosis: 49 versus 59 yr; P < 0.0001; risk ratio, 3.2; hypertension: 51 versus 65 yr; P < 0.0001; risk ratio, 4.4). Similarly, those who had an episode of gross hematuria before age 30 had a worse renal outcome than those who did not (49 versus 59 yr; P < 0.0001; risk ratio, 2.6). We have also calculated risk ratios for a combined model. When therapeutic interventions become available for this disease, these populations with high risk ratios should be considered for such interventions.

Nephrogenic Adenoma of the Urethra Presenting as Gross Hematuria in a Child

A 15-year-old boy presented with intermittent blood spotting on the underwear and 1 episode of gross hematuria associated with dysuria. Urinalysis revealed 1 to 3 red blood cells per high power field. Kidney and bladder ultrasound, excretory urography and retrograde urethrography were normal. Cystoscopy revealed normal bladder findings and 3 small yellowish polypoid structures on the ventral and left lateral walls of the bulbous urethra, which were biopsied and fulgurated. Biopsies revealed nephrogenic adenoma (see figure). Hematuria has not recurred postoperatively.

Intravesical Methylmethacrylate After Revision Hip Arthroplasty

Intrapelvic extrusion of cement during total hip replacement is common but complications are infrequently reported. Tissues affected by intrapelvic cement include bowel, vessels, nerves, ureters and bladder.' We report a case of 2 pieces of cement eroding sequentially into the bladder 5 years after right total hip replacement revision. CASE REPORT A 66-year-old woman with a history of congenital hip dysplasia, bilateral total hip replacements and revision of the right hip replacement in 1989 presented with recurrent afebrile urinary tract infections and intermittent episodes of gross hematuria 4 months in duration. Urine cultures yielded Escherichia coli and the patient responded to oral antibiotics. Anteroposterior radiography of the right hip confirmed stable protrusio from the revision site but no opacity was identified in the bladder region. Excretory urography showed medial deviation of the right ureter but no opacity in the bladder. Cystoscopy revealed a calcified mass in the right portion of the bladder. Open cystolithotomy was performed. A 5 cm. piece of orthopedic cement was seen eroding through the right lateral bladder wall (see figure). Attempts to mobilize the bladder from the right pelvic side wall were unsuccessful due to adhesions secondary to multiple orthopedic surgery. Via an intravesical approach the cement was removed using circumscribing excision. The perivesical space and defect in the Accepted for publication May 24, 1996. bladder wall were inspected, and no remaining cement was detected. Convalescence was uneventful. Eight months after surgery the patient complained of right lateral leg pain and urinary tract infections that did not resolve with antibiotics. An arthrogram showed a flow of contrast material from the right total hip replacement site into the perivesical space. Aspirated sinovial fluid and urine culture yielded group D Enterococcus. Repair of this fistula revealed a new piece of cement in the bladder wall. Partial cystectomy was performed to repair the bladder with omentum brought down to barricade the bladder from the medial wall of the implant. After 18 months the patient is mobile with the right hip and has no urinary complaints. DISCUSSION

Don't forget sickled cells in the urine when investigating a patient for haematuria

Haematuria is a well-known complication of sickle cell disease. A South African coloured patient with repeated episodes of gross haematuria is described in whom the diagnosis of sickle cell disease was suggested after the finding of sickled erythrocytes in the urine sediment. The diagnosis was then confirmed by haemo globin electrophoresis, which revealed sickle cell trait (Hb-AS). It is concluded that sickled erythrocytes must be looked for when urine is microscopically scrutinized to determine the source of a haematuria.

Orbital Metastasis From a Urachal Tumor

The urachus is a vestigial remnant that, in the midgestational period, connects the umbilicus to the apex of the urinary bladder. Hue and Jacquin 1 described the first case of carcinoma arising from the urachal remnant in 1863. More than 200 cases have been subsequently reported. The incidence of urachal malignancy is reported to be less than one in 1000 bladder tumors. 2 Patients usually present with urinary symptoms, such as hematuria or dysuria. Histologically, mucin-secreting adenocarcinoma is the most common type of urachal malignant disease. 3 Distant metastases, when they occur, usually involve lung or bone; however, metastases to the parieto-occipital 3 and occipital lobes of the brain 4 have been reported. We describe herein a patient with urachal carcinoma that metastasized to the orbit. Report of a Case. In September 1990, a 28-year-old white woman noted recurrent episodes of gross hematuria. Cystoscopy revealed an ulcerating tumor at the

Loin pain-hematuria syndrome associated with thin glomerular basement membrane disease and hemorrhage into renal tubules

Loin pain-hematuria (LPH) syndrome is a poorly understood disorder in which the patients, mainly young women, experience unexplained severe chronic unilateral or bilateral flank pain associated with gross and/or microscopic hematuria. By contrast, thin glomerular basement membrane (GBM) disease is generally thought to be a benign disorder, affecting males and females equally, in which the major manifestation is asymptomatic microscopic hematuria. Herein we describe seven patients (6 females, 1 male) in whom thin GBM appeared to be the cause of the LPH syndrome. The gross hematuria in these patients could be attributed to thin GBM disease because the renal biopsy demonstrated red cells in renal tubules (indicating glomerular hematuria) and the only glomerular abnormality present with thin GBM. In addition, the other causes of gross hematuria were excluded by appropriate testing. The flank pain in these patients might also have been the result of their thin GBM disease. This is suggested by renal biopsy findings of multiple renal tubules filled with red cells, apparently occluding the tubules. We suggest that occlusion of a relatively small fraction of renal tubules could cause renal pain if back-leak of glomerular filtrate occurred that was of sufficient magnitude to expand renal parenchymal volume and stretch the renal capsule. Preliminary observations suggest that treatment with the angiotensin converting enzyme (ACE) inhibitor enalapril importantly reduces the frequency and severity of the episodes of gross hematuria and flank pain in most patients. ACE inhibition might decrease glomerular hemorrhage in patients with think GBM by decreasing glomerular hydrostatic pressure. We conclude that (1) Thin GBM disease can be the cause of gross hematuria, apparently as a result of rupture of thin GBM. (2) Rupture of thin GBM resulting in hemorrhage into renal tubules may be the cause of the flank pain and gross hematuria in some patients with the LPH syndrome.

Renal Aneurysms and IgA Nephropathy

Letters15 November 1995Renal Aneurysms and IgA NephropathyEmanuela Cecchin, MD, Sergio De Marchi, MD, and Ettore Bartoli, MDEmanuela Cecchin, MDUniversity of Udine Medical School; Udine, ItalySearch for more papers by this author, Sergio De Marchi, MDUniversity of Udine Medical School; Udine, ItalySearch for more papers by this author, and Ettore Bartoli, MDUniversity of Udine Medical School; Udine, ItalySearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-10-199511150-00022 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:We describe a patient with previously diagnosed IgA nephropathy presenting with persistent macrohematuria and iron-deficiency anemia, in whom angiography showed multiple bilateral renal aneurysms.In January 1993, a 31-year-old woman was hospitalized because of persistent macrohematuria and moderate iron-deficiency anemia. She did well until 1987, when she experienced two episodes of gross hematuria. A percutaneous renal biopsy specimen showed a moderate focal and segmental mesangial proliferation associated with a discrete increase in the mesangial matrix in 75% of the glomeruli. Tubulointerstitial changes were minimal, and there was no evidence of vasculitis. The immunopathologic pattern was characterized by ...

Hypercalciuria and nephrocalcinosis, a feature of Wilson's disease

Hypercalciuria and nephrocalcinosis are not uncommon in patients with Wilson's disease but have only once been reported as the presenting sign. We diagnosed Wilson's disease in a 17-year-old male patient 6 years after his first episode of gross hematuria and 2 years after detection of hypercalciuria and nephrocalcinosis. Therapy with penicillamine resulted only in a moderate reduction of urinary calcium excretion but oxalate excretion increased.