Lectin Peroxidase Conjugate Reactivity in Acquired Cystic Disease of the Kidney

Ishikawa, Isao; Horiguchi, Takayasu; Shikura, Naoto

doi:10.1159/000185287

Cited by 15 publications

(10 citation statements)

References 4 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Ishikawa et al [18]reported that single-layered epithelial cells in acquired cysts were positive for tetragonolobus lectin in 92.2% and multilayered epithelial cells were positive for tetragonolobus lectin in 88% and revealed a low positive number of peanut lectin. This result suggested that acquired cysts are derived from proximal cysts.…”

Section: Discussionmentioning

confidence: 99%

Incidence of Acquired Renal Cysts in Biopsy Specimens

Liu

Ishikawa

Horiguchi

2000

Nephron

Self Cite

View full text Add to dashboard Cite

Aims: This study investigated whether or not acquired renal cysts develop in patients with mild chronic renal failure. Methods: A retrospective study was carried out using renal biopsy specimens from 720 patients. A renal cyst was defined as a tubule dilated >200 µm. Results: Renal cysts were found in 21 of 720 renal biopsy specimens. Serum creatinine of 21 patients with renal cysts was significantly higher than that of 699 patients without cysts (2.59 ± 2.64 vs. 1.09 ± 0.79 mg/dl) (p < 0.0001). Poor renal function (serum creatinine >1.6 mg/dl) reveals more cyst formation on biopsy specimens than good renal function (serum creatinine <1.5 mg/dl). Cysts were observed in 11 of 607 (1.8%) patients less than 50 years of age and in 10 of 113 (8.8%) patients over 51 years. To exclude simple cysts which are commonly observed in older subjects, 11 patients under 50 years of age were extensively examined. Mean serum creatinine was 2.98 ± 3.06 mg/dl (0.7–10.4 mg/dl). These 11 patients revealed low creatinine clearance of 47.5 ± 25.6 ml/min (5–71 ml/min). Creatinine clearances in 7 patients were 52–71 ml/min (serum creatinine 0.7–2.0 mg/ dl). One of 11 biopsy specimens with cysts was examined by immunohistochemistry on lectin. This specimen was positive for tetragonolobus lectin and negative for peanut lectin, suggesting that the epithelial cells lining the cyst were derived from proximal tubules, unlike those of simple cysts. Conclusion: These results suggest that low normal renal function such as creatinine clearances 52–71 ml/min due to nephron loss is sufficient to induce acquired cyst development in various renal diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

Incidence of Acquired Renal Cysts in Biopsy Specimens

Liu

Ishikawa

Horiguchi

2000

Nephron

Self Cite

View full text Add to dashboard Cite

show abstract

“…Interestingly, at 12 months of age, the percentage of PT cysts increased as compared with that at 3 months, from 15% to 29%; however, most of the PT cysts corresponded to mildly dilated tubules, whereas the majority of larger cysts were either of CD origin (56%, 13.6% of area) or dedifferentiated (15%, 8.5% of area; Figure 6, A and C, and Table 1). The PT dilatation at this stage may reflect acquired renal cystic disease associated with advanced renal insufficiency as seen in human ADPKD (74,75).…”

Section: Figurementioning

confidence: 96%

Functional polycystin-1 dosage governs autosomal dominant polycystic kidney disease severity

et al. 2012

View full text Add to dashboard Cite

Autosomal dominant polycystic kidney disease (ADPKD) is caused by mutations to PKD1 or PKD2, triggering progressive cystogenesis and typically leading to end-stage renal disease in midlife. The phenotypic spectrum, however, ranges from in utero onset to adequate renal function at old age. Recent patient data suggest that the disease is dosage dependent, where incompletely penetrant alleles influence disease severity. Here, we have developed a knockin mouse model matching a likely disease variant, PKD1 p.R3277C (RC), and have proved that its functionally hypomorphic nature modifies the ADPKD phenotype. While Pkd1 +/null mice are normal, Pkd1 RC/null mice have rapidly progressive disease, and Pkd1 RC/RC animals develop gradual cystogenesis. These models effectively mimic the pathophysiological features of in utero-onset and typical ADPKD, respectively, correlating the level of functional Pkd1 product with disease severity, highlighting the dosage dependence of cystogenesis. Additionally, molecular analyses identified p.R3277C as a temperature-sensitive folding/ trafficking mutant, and length defects in collecting duct primary cilia, the organelle central to PKD pathogenesis, were clearly detected for the first time to our knowledge in PKD1. Altogether, this study highlights the role that in trans variants at the disease locus can play in phenotypic modification of dominant diseases and provides a truly orthologous PKD1 model, optimal for therapeutic testing.

show abstract

“…As regards the origin, cystic adenomatous lesions in our animal model developed from basophilic cell tubules that were presumably derived from the proximal nephrons [14]. Most neoplastic lesions found in human ACDK were also thought to arise from the proximal nephrons [15]. Therefore, DPT-induced cystic lesions in rat kidney bear a close resemblance to human ACDK in terms of origin as well as pathological appearances.…”

Section: Discussionmentioning

confidence: 99%

A Rat Model of Chemical-Induced Polycystic Kidney Disease with Multistage Tumors

Ito

Toma

Yamaguchi

et al. 1998

Nephron

View full text Add to dashboard Cite

Diphenylthiazole (DPT) induces polycystic kidney disease in the rat which serves as a model of human acquired cystic disease of the kidney. However, DPT administration alone does not produce neoplastic changes in renal cysts. We examined the effect of N-nitrosomorpholine (NNM), a carcinogen, in rats bearing DPT-induced renal cysts. Forty Sprague-Dawley rats were divided into four groups: DPT/NNM, DPT, NNM, and nontreated groups. DPT was administered throughout the experimental period, and NNM was given from weeks 4 to 7 after the start of the experiment. The rats were sampled from weeks 39 to 48, and histopathological examinations of the excised kidneys were performed. Multiple cystic changes were observed in all the DPT-treated rats in both DPT and DPT/NNM groups which were absent in almost all other rats. Solid adenomatous lesions were observed in the NNM-treated rats: in 7 of 9 and in 3 of 10 rats in the DPT/NNM and NNM groups, respectively. Cystic adenomatous lesions were found in 4 of 9 rats in the DPT/NNM group exclusively and not in the other groups. Combined DPT and NNM administration to rats produced an animal model showing neoplastic changes in renal cysts resembling microscopically renal cancer lesions in human acquired cystic disease of the kidney (on hematoxylin and eosin staining).

show abstract

Lectin Peroxidase Conjugate Reactivity in Acquired Cystic Disease of the Kidney

Cited by 15 publications

References 4 publications

Incidence of Acquired Renal Cysts in Biopsy Specimens

Incidence of Acquired Renal Cysts in Biopsy Specimens

Functional polycystin-1 dosage governs autosomal dominant polycystic kidney disease severity

A Rat Model of Chemical-Induced Polycystic Kidney Disease with Multistage Tumors

Contact Info

Product

Resources

About