Persistent Microscopic Hematuria Research Articles

Idiopathic IgA Mesangial Nephropathy

Histological features and data on the natural history after 1 to 45 years (mean 6.56 +/- 8.55) of total apparent duration and 1 to 13 years (mean 3.48 +/- 5.04) of post-biopsy follow-up, are reported in 374 patients (mean age, 33.9 +/- 11.9 yrs) with idiopathic mesangial IgA nephropathy, who presented with a history of macroscopic hematuria (56%), recurrent in two-thirds of the patients, or with persistent microscopic hematuria and no previous episodes of gross hematuria (44%). Mesangial cell proliferation ranged from minimal to diffuse. Associated varying degrees of extracapillary proliferation, segmental and global glomerular sclerosis, tubulo-interstitial damage and arteriolar hyalinosis usually correlated with each other and with the extent of mesangial proliferation (P less than 0.05). The actuarial curve of progression to renal death showed a 75% survival after 20 years from apparent onset. Progression to renal failure was more rapid in patients with: an older age at onset (P = 0.0582); male sex (P = 0.0730); no history of recurrent gross hematuria (P = 0.0406); high blood pressure (P = 0.0011); more marked global (P = 0.0007) and segmental (P = 0.0026) glomerular sclerosis; more severe interstitial sclerosis (P = 0.0147); more diffuse and global mesangial proliferation (P = 0.0820); mesangio-parietal pattern at immunofluorescence (P = 0.0778). However, all these parameters showed a poor predictive value if applied to any single patient.

The thin glomerular basement membrane in children with haematuria.

To determine the specificity and significance of widespread attenuation of the glomerular basement membrane on electron microscopy, 240 renal biopsies from 218 children were studied retrospectively. Twenty-three patients showed diffuse attenuation and three of them are cases of hereditary nephritis. The other 20 patients are characterized by persistent microscopic haematuria, absence of proteinuria, normal blood pressure and renal function, and minimal glomerular changes. In 10 of these 20 children, microscopic haematuria was also present in the family. We conclude that widespread attenuation of the glomerular basement membrane is a characteristic of benign familial and non-familial haematuria. The thin glomerular basement membrane may be responsible for the haematuria and may result from incomplete glomerular maturation.

Renal Histological Studies in Patients with Takayasu’s Arteritis

Clinical findings and structural alterations of the kidney in 3 patients with Takayasu's arteritis (TA) and associated glomerulonephritis are described. Clinical evidence of renal disease included persistent proteinuria and microscopic hematuria in all patients. Renal histology showed proliferative glomerulonephritis in 2 of the 3 patients. In 1 patient in whom sequential examination of the kidney was possible, glomerular changes had progressed in severity, in parallel with the expansion of arterial damage of TA. Prednisolone therapy induced a complete disappearance of systemic symptoms of TA and an improvement of proteinuria and hematuria. These findings suggest that TA, which quite possibly results from an immune response to disseminated antigen(s), may occasionally induced glomerulonephritis as a part of its histological expression.

Cushing's Disease in a Patient With an Ectopic Pituitary Adenoma

THE OCCURRENCE of pituitary tissue in an ectopic location but not in continuity with intrasellar pituitary tissue has been previously reported.^1-7However, pituitary dysfunction in such patients is uncommon.^1-3We describe here a patient with pituitary-dependent Cushing's syndrome who had a chromophobe adenoma located in the sphenoid sinus. <h3>Report of a Case</h3> A 51-year-old woman was admitted to our medical center in 1976 for evaluation of persistent microscopic hematuria. This was first noted two years earlier on routine urinalysis and on repeated examinations. Findings from renal function tests, intravenous pyelogram, and cystoscopy were considered normal. She was known to have arterial hypertension for at least five years. Her blood pressure (BP) responded favorably to medication until three months before admission, when it became difficult to control. During this period the patient noted increasing weakness, malaise, puffiness of her face, facial hair, increasing skin pigmentation, and weight gain. Her

Transurethral Resection of the Prostate with Partial Resection of the Seminal Vesicle

A retrospective study was done on 185 patients who underwent transurethral prostatectomy. Of these patients 6 had seminal vesicle tissue in the resected specimen. The presence of the yellow-brown pigment, lipofuscin, in the seminal vesicle epithelium was a consistent finding and, often, paramount to differentiation from carcinoma of the prostate. There was no pathological misdiagnosis of malignancy in this series. Of the 6 patients 2 suffered acute epididymitis postoperatively and 1 had persistent microscopic hematuria 2 months postoperatively. The high incidence of postoperative epididymitis probably is owing to contamination of the seminal vesicles by bacteria, acquired during urinary tract manipulation, having access to the seminal vesicles and, thus, the vas deferens. In these patients vasectomy and broad-spectrum antibiotics are recommended because epididymal invasion by bacteria may already have occurred before pathologic diagnosis is obtained.

IgA glomerulonephritis. Mesangial IgA deposition without systemic signs (Berger's disease).

Renal biopsy specimens from 204 patients with glomerulonephritis or nephrotic syndrome have been studied. In ten of the patients not suffering from acute poststreptococcal glomerulonephritis, systemic lupus erythematosus or Schönlein-Henoch syndrome, diffuse, selective mesangial IgA deposition was observed. Clinically, persistent microscopic haematuria, mild proteinuria and, except in one patient, normal renal function were found. Light microscopically the histological picture was dominated by a diffuse or focal increase in volume of the mesangial matrix, and mild mesangial cell proliferation. Exceptionally, there was also crescent formation. Immunofluorescence revealed large IgA, IgG and C3 deposits, as well as small IgM and fibrinogen deposits in the mesangial glomeruli. The authors' assumption that immunocomplexes containing a secretory component might be implicated in the pathomechanism of Berger's disease, could not be proved.

IgA–IgG Nephropathy: A Clinicopathologic Entity with Slow Evolution and Favorable Prognosis

Renal biopsy specimens were obtained from nine patients with proteinuria and persistent macroscopic or microscopic hematuria. Histologic examination either disclosed no abnormality or showed moderate mesangial thickening and occasionally, evidence of focal segmental glomerulonephritis. Immunofluorescent studies revealed diffuse generalized mesangial deposits of IgA, IgG and betalc in all specimens. Fibrinogen deposits were present in the mesangial space in four specimens only, while IgM was uniformly absent. Serial sections of identical glomeruli allowed the localization of betalc within both IgA and IgG deposits. Ultrastructural studies of the renal biopsy specimens showed accumulation of electron-dense material in the subendothelial region of the capillary loops and the mesangium, with thickening of its matrix. Follow-up data indicated a generally good prognosis.

Focal segmental glomerulosclerosis

In this clinicopathologic study of 16 cases of focal segmental glomerulosclerosis, the median age at onset was 21 years. Sixty per cent had persistent microscopic hematuria, 88 per cent had the nephrotic syndrome, and all had steroid-resistant proteinuria. The clinical course was not affected by corticosteroid or immunosuppressive agents. Typical juxtamedullary focal segmental sclerotic lesions were found in 88 per cent of the initial renal biopsy specimens. The sclerotic glomerular lesions contained immunofluorescent deposits of immunoglobulin M (IgM), C′3 and C′4. Electron dense deposits were identified in the sclerotic glomerular segments. Because of the different morphologic and immunologic findings and the grave prognosis, focal segmentai glomerulosclerosis should be differentiated from lipoid nephrosis.

Recurrent or Persistent Hematuria

Renal biopsies were performed on 47 patients with recurrent macroscopic or persistent microscopic hematuria, unexplained by urinary-tract abnormalities or manifest renal disease. Histologic examination showed a mesangial proliferative glomerulonephritis in 34 patients. Granular deposits of immunoglobulins and complement components were present in the glomerular mesangial area in 15 of 24 biopsies examined by immunofluorescence technics. IgM, β1C and C1q were deposited in all patients, IgA in 10 patients, and IgG in only two. The intensity of immunofluorescent staining correlated with the glomerular proliferate reaction as judged by light microscopy. Electron-dense granular deposits in the mesangial area were found exclusively in patients with active disease. Thus, the glomerulonephritis in these patients was caused by an IgM and IgA antibody-associated mesangial immune-complex deposition with activation of the classic complement pathway. Follow-up data in 41 patients and repeated renal biopsies in 11 patients indicate a good prognosis. (N Engl J Med 290:1165–1170, 1974)

Familial Benign Essential Hematuria

The hereditary features of renal disease have engendered much interest since the turn of the century. Hereditary cystic renal disease, abnormalities in both proximal and distal tubular function, chronic glomerulonephritis, nephrosis, congenital anomalies, and tumors of the genitourinary tract are well documented and were the subject of a recent review by Perkoff.¹ This paper describes a family with persistent microscopic hematuria of glomerular origin without nephritis, deafness, ocular lesions, impairment of renal function, or other congenital anomalies. An unusual structural abnormality, thin glomerular capillary basement membranes, was a constant finding in this kindred and may be the cause of the hematuria. Hematuria is usually considered a serious symptom, and its presence calls for meticulous investigation. The diagnosis of "idiopathic" or "essential" hematuria is a diagnosis of exclusion, and can be made only when no cause for the hematuria is found after exhaustive investigation. The abnormality causing the hematuria can

"Benign" hematuria with focal glomerulitis in adults.

Pediatricians have reported benign hematuria owing to focal glomerulitis of unknown cause in children with normal blood pressure and glomerular filtration rates. Because a few reports have suggested that a similar benign syndrome occurs in adults, we undertook a prospective and retrospective study of 21 patients, ages 14 to 41 years, who initially fulfilled the following criteria: recurrent or persistent gross or microscopic hematuria, normal blood pressure, normal serum creatinine level and creatinine clearance, 24-hour urine protein excretion not exceeding 1 g, absence of known causes of glomerulonephritis or nonglomerular causes of hematuria, and renal biopsy changes of focal, local glomerular hypercellularity. Eighteen patients were reevaluated 0.83 to 11 years after the first episode of hematuria. Of these, 13 had persistent hematuria, but in only 1 patient had 24-hour protein excretion risen, from 790 mg to 2.2 g. Five of those re-evaluated had normal urinalyses and protein excretion. In all patients reevaluated blood pressure, serum creatinine levels and creatinine clearance were normal. The short-term prognosis (2 to 10 years) is therefore excellent for adults with hematuria, minimal proteinuria, and idiopathic focal glomerulitis who have normal blood pressure and renal function.

BENIGN FAMILIAL HEMATURIA

Asymptomatic persistent renal hematuria of 6 months to 8 years' duration was observed in seven of eight siblings. There was no family history of renal disease or deafness, and other family members examined showed normal urinalyses; none of the other known forms of hereditary renal disease were detected. Abnormalities of renal function or general physical health and development were not detected. Renal biopsies were performed in the two patients with the longest history of hematuria (7 and 8 years). Light and immunofluorescence microscopic study of renal tissue revealed no abnormalities of glomeruhi or interstitial tissue. This familial condition is characterized by persistent microscopic hematuria with episodic gross hematuria and a favorable long-term prognosis. Although the pathogenesis is unclear, an immune process does not appear to be involved. Microscopic examination of the urine of family members in hematuria without an obvious etiology is warranted.