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S J Wahl

Publications and source records attributed to S J Wahl.

9 recordsLinked to original sources

Increasing incidence of focal segmental glomerulosclerosis and an examination of demographic patterns.

BACKGROUND: Idiopathic focal segmental glomerulosclerosis (FSGS) is one of the leading causes of the nephrotic syndrome in adults and an important cause of end-stage renal disease. Its incidence has dramatically increased in the last two decades and it is especially prevalent among black patients. The trend of FSGS incidence has not been reported beyond 1997. METHODS: We retrospectively reviewed all renal biopsies performed at our institution between 1986 and 2002 and identified patients with diagnoses consistent with primary glomerulopathy (PG), which included: minimal-change disease (MCD), idiopathic focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MGN), IgA nephropathy (IgA), membrano-proliferative glomerulonephritis (MPGN) and mesangioproliferative glomerulonephritis. Patients with possible secondary causes for their renal disease were excluded. Clinical data at the time of biopsy and follow-up data were collected and analyzed. RESULTS: During the period from January 1986-December 2002, 299 renal biopsies were performed and 132 patients were diagnosed with PG. FSGS was the most common form of PG representing 37.8% of all PG followed by IgA 27.3%, MGN 16.6% and MCD 9.1%. Among FSGS patients 59% were females, 64% had nephrotic range proteinuria and 54% had the nephrotic syndrome. Mean serum creatinine was 2.0 +/- 0.2 mg/dl and mean protein excretion was 6.1 +/- 1.0 g/day. The incidence of FSGS increased from 19.3% (1986-1991) and 16.6% (1992-1997) to 58.5% in the period from 2002. The increase occurred among black and Hispanic patients (33.3-79.2%) as well as white patients (12.5-51.5%). Black and Hispanic patients with PG presented for renal biopsy at a significantly younger age than white patients (p = 0.003), with mean age 37.5 +/- 2.0 years vs. 50.3 +/- 1.8 years. White FSGS patients were significantly older than white non-FSGS patients (mean age 56.4 +/- 3.2 years vs. 48.0 +/- 2.0 years, p = 0.03). Black and Hispanic FSGS patients were also older when compared to their non-FSGS counter-parts (mean age 40.6 +/- 2.8 years vs. 32.1 +/- 2.0 years, p = 0.04). When patients were stratified by age (< 45 years and > or = 45 years), FSGS was the most common diagnosis in both age groups among black and Hispanic patients (55.1% and 88.8%) but only among older white patients (36.2%). CONCLUSIONS: The incidence of FSGS as a proportion of PG in our population has increased markedly in the most recent time period analyzed (1998-2002). The increase has occurred among both white and black and Hispanic patients. We also found that FSGS was most prevalent in patients > or = 45 years.

Age Factors↗

Carbohydrate antigen 19-9 and carcinoembryonic antigen immunostaining in benign multicystic mesothelioma of the peritoneum.

A 58-year-old Italian man was incidentally discovered to have an elevated carbohydrate antigen 19-9 (CA-19-9) level of 132 U/mL on routine blood testing. Multisystem imaging studies revealed multiple benign-appearing cysts of the liver and single cysts in the pancreas and kidney parenchyma. Throughout 14 months, fluctuations were observed in the elevated serum CA-19-9 levels from 99 to 450 U/mL. Serum carcinoembryonic antigen (CEA) and other tumor markers were normal. Laparoscopy disclosed multiple cystic lesions on the surface of the liver, on the serosal surface of the ileum, and in the mesentery. Electron microscopy characterized the cells as mesothelial. The pathologic diagnosis was benign multicystic mesothelioma of the peritoneum (BMMP). Aspirated fluid from the liver cyst revealed CA-19-9 levels at 28 500 U/mL, strongly linking the elevated serum CA-19-9 levels with mesothelial cyst secretion. Immunostaining was positive for CA-19-9, CEA, and cancer antigen 125 (CA-125). We believe this is the first documented instance of CA-19-9 and CEA secretion in BMMP.

CA-19-9 Antigen↗

Papillary mucinous adenoma arising in adenomyomatous hyperplasia of the gall bladder.

A case of papillary mucinous adenoma arising in adenomyomatous hyperplasia (AMH) of the gall bladder is reported. The lesion was unsuspected and discovered by routine palpation of the gall bladder during laparotomy. The adenoma developed within fundal AMH and showed cytological atypia. This case illustrates that neoplastic proliferation is indeed possible in AMH and challenges the classical opinion that AMH is devoid of neoplastic potential.

Adenoma↗

Cholesterol crystal embolization-associated renal failure after therapy with recombinant tissue-type plasminogen activator.

We report the occurrence of renal failure due to cholesterol crystal embolization following thrombolytic therapy with intravenous recombinant tissue-type plasminogen activator (t-PA). No invasive vascular procedure had been performed. Although there is one case report of cholesterol crystal embolization following t-PA therapy with only extrarenal manifestations (N Engl J Med 321:1270, 1989), this is the first reported case of atheroembolic acute renal failure following t-PA therapy.

Acute Kidney Injury↗

p53 expression in precancerous gastric lesions: an immunohistochemical study of PAb 1801 monoclonal antibody on adenomatous and hyperplastic gastric polyps.

To determine the chronology of p53 mutation in the gastric carcinogenic sequence, we studied p53 overexpression in premalignant lesions, including 17 adenomatous polyps (10/17 surrounded by intestinal metaplasia and 11/17 harboring foci of adenocarcinoma or severe dysplasia), and 18 hyperplastic polyps (4/18 with focal adenomatous changes). Immunohistochemistry with PAb 1801 monoclonal antibody was performed on archival material; p53 nuclear staining was seen in 10/17 adenomas, but was limited to the foci of adenocarcinoma in three cases. Five adenomas with foci of severe dysplasia or carcinoma were nonreactive. Intestinal metaplasia, normal gastric mucosa, and 14/18 hyperplastic polyps were nonreactive. p53 Reactivity observed in four hyperplastic polyps was limited to adenomatous foci. These results suggest that p53 overexpression occurs in dysplastic epithelium of precancerous gastric lesions. Its absence in chronic atrophic gastritis with intestinal metaplasia suggests it is a relatively late event in the gastric carcinogenic sequence.

Adenocarcinoma↗