Contributing factors for fever after tubeless percutaneous nephrolithotomy.

OBJECTIVE: To evaluate the contributing factors for fever after tubeless percutaneous nephrolithotomy (PCNL). METHODS: Between May 2009 and December 2013, 395 tubeless PCNLs were performed at our hospital. After stone extraction, the bleeding points were cauterized for hemostasis to enable tubeless modification. In patients with troublesome bleeding after cauterization, oxidized regenerated cellulose (Surgicel) strips were used to tamponade the access tract to facilitate bleeding control. The contributory factors for fever were evaluated by a retrospective chart review. RESULTS: Forty-four patients (11.7%) developed fever after tubeless PCNL. There was no difference in gender, age, and body mass index in the development of fever. Episodes of febrile or septic urinary tract infection before PCNL were found to have occurred in 35 patients, but the incidence of postoperative fever was not significantly higher in these patients. There is no significant difference in the mean stone size in fever and nonfever patients. Complete staghorn stones were noted in 40 patients, and their fever rate was not significantly higher than patients with nonstaghorn stone. The operation time is not significantly higher in the group with urinary tract infection. Patients with postoperative fever had a high incidence of residual stones than the remaining patients (38.9% vs 20.4%). There was no significant difference in incidence of postoperative fever in patients with struvite stones than patients with nonstruvite stones. In patients who received Surgicel packing, the incidence of fever was not significantly higher. CONCLUSION: Incomplete stone extraction is a major contributing factor for the development of fever after tubeless PCNL.

Age-dependent association between Dickkopf-1 and calcium-containing urolithiasis.

OBJECTIVE: To evaluate the serum Dickkopf-1 (DKK1) level in patients with calcium-containing upper urinary tract stones (Ca-UUTS). METHODS: The study retrospectively enrolled 184 patients with Ca-UUTS and 46 age-matched controls. The serum DKK1 level and urine calcium/creatinine ratio were detected in both groups. RESULTS: The mean serum DKK1 level in the controls was 321.7 ± 284.1 pg/mL, which was significantly lower than that of the patients with calcium oxalate and calcium phosphate (CaOx + CaP), CaOx, and CaP stones (687.8 ± 600.2, 640.5 ± 721.5, and 857.9 ± 913.2 pg/mL, respectively). The mean urine calcium/creatinine ratio, an indicator of hypercalciuria, was higher in the Ca-UUTS patients with CaOx + CaP (0.10 ± 0.06), CaOx (0.13 ± 0.07), and CaP (0.12 ± 0.07) stones than in the controls (0.08 ± 0.04). Statistical significance was noted only in the patients with CaOx (P = .005) and CaP (P = .037) stones. A significant positive association was found between the serum DKK1 level and age in the control group but not in the Ca-UUTS patients. In subjects aged younger than 50 years, the serum DKK1 level in the Ca-UUTS group was significantly higher than in the control group (605.3 ± 514.4 vs 274 ± 229.8 pg/mL, P = .0003). The serum DKK1 level was not associated with stone size. CONCLUSION: Serum DKK1, an inhibitor of the Wnt signaling pathway, was positively associated with the formation of Ca-UUTS, especially in patients aged younger than 50 years.

Mass spectrometric study of stone matrix proteins of human bladder stones.

OBJECTIVE: To evaluate the mechanisms of bladder uric acid stone (BUAS) formation by analyzing BUAS stone matrix proteins, with mass spectrometry (MS). MATERIALS AND METHODS: Stone matrix proteins were extracted from 5 pure BUASs. The obtained proteins were analyzed with reverse phase liquid chromatography-tandem MS. The acquired data were investigated against a Swiss Prot human protein database, using Matrix Science Mascot. The identified proteins were submitted to UniProtKB website for gene ontology analysis to define their correlation. They were also submitted to Metacore platform and Kyoto Encyclopedia of Genes and Genomes website for pathway analysis. MS-determined protein expressions were validated by immunoblot. RESULTS: The liquid chromatography-tandem MS analysis identified 58-226 proteins in the 5 BUASs (450 proteins). Metacore software analysis suggests that inflammation might play an important role for BUAS formation. The analysis of endogenous metabolic pathways revealed that these proteins were categorized into glycerophospholipid or glycosphingolipid biosynthesis. Four of 5 identified proteins selected for validation, including uromodulin, S100P, Histone 4, and nucleophosmin, can be validated in the immunoblot data. CONCLUSION: Our results suggest that inflammatory process and lipid metabolism might play a role in the formation of BUAS. Whether these inflammatory responses are the etiology of stone formation or whether they result from local damage by stone irritation is uncertain.

Proteomic study of renal uric acid stone.

OBJECTIVE: To analyze urinary uric acid stone matrix proteins (SMP) with mass spectrometry (MS) to evaluate the mechanisms of uric acid stone formation. SMP plays an important role in urinary stone formation. Several proteomic studies apply to calcium-containing stones have been reported; however no proteomic study for urinary uric acid stone has been reported. METHODS: Pure kidney uric acid stones from 5 individuals were demineralized, and SMPs were isolated. The obtained proteins were analyzed with reverse-phase liquid chromatography-tandem MS. The acquired data were searched against a Swiss Prot human protein database using Matrix Science, Mascot. The identified proteins were submitted to the AmiGO Web site for gene ontology analysis. They were also sumitted to Metacore software and Kyoto Encyclopedia of Genes and Genomes website (KEGG) for pathway analysis. MS-determined protein expressions were verified by immunoblot. RESULTS: MS analysis identified 242 proteins from 5 proteomic results and the number of the identified protein of each result ranged from 52 to 156. Metacore software analysis suggested that inflammation may play an important role for kidney uric acid stone formation. Endogenous metabolic pathways were also analyzed and submitted to KEGG Web site, which revealed that these proteins may participate in fat metabolism. Five identified proteins were selected for immunoblot validation, and 3 proteins were confirmed. CONCLUSION: Our results suggest that inflammatory process may play a role in kidney uric acid stone formation. Our endogenous metabolic pathway analysis data revealed that these proteins may participate in lipid metabolism. Whether this finding implies a relation between lipotoxicity and kidney uric acid stone former requires further investigation.