Cyst infection in autosomal dominant polycystic kidney disease: our experience at Toranomon Hospital and future issues

Abstract

Cyst infection is a frequent and serious complication of autosomal dominant polycystic kidney disease (ADPKD) that is often difficult to treat and can be fatal. However, much is still unknown about cyst infection. Positron emission tomography (PET) is generally recommended for detecting infected cysts, but it has the disadvantages of limited availability, high cost, and radiation exposure. We have devised magnetic resonance imaging (MRI) diagnostic criteria for cyst infection. Lipid-soluble antibiotics such as fluoroquinolones show good penetration into cysts and are recommended for cyst infection. However, we reported that fluoroquinolone-resistant microorganisms showed a high prevalence in cyst infection. We should, therefore, reconsider the empirical use of fluoroquinolones for ADPKD patients with cyst infection. We have suggested a new antibiotic strategy according to the severity of cyst infection. It may be important to consider the drug half-life in serum in addition to the drug susceptibility when selecting antibiotics Cyst drainage is necessary for some patients with refractory cyst infection; however, cyst drainage can be associated with severe adverse events. We suggest adaptation criteria for cyst drainage in patients with cyst infection in ADPKD. Most causative bacteria of cyst infection are enterobacteria, and hematogenous spread via bacterial translocation in the intestine is considered the main cause of cyst infection. Therefore, intestinal flora may be important for cyst infection. The role of the intestinal flora in cyst infection in ADPKD is unknown and should be explored in future research.

Repetitive Refractory Renal Cyst Infection in Autosomal Dominant Polycystic Kidney Disease for which Renal Transcatheter Arterial Embolization Was Effective in Preventing Recurrence

“…The second finding was that renal TAE might have prevented recurrence of renal cyst infection in this patient. Theoretically, hematogenous bacterial spread can be prevented by shutting down the renal blood flow by renal TAE (6,11,12). This case supported this hypothesis.…”

“…These antibiotics may not penetrate infected renal cysts with heavily calcified wall thickening, which might be why meropenem was not very effective in this case. It may also be important to consider the drug half-life in serum in addition to the drug susceptibility when selecting antibiotics (11). The time above the minimum inhibitory concentration (MIC) is an important determinant of the activity of βlactams.…”

“…This case was not considered to have a severe cyst infection on admission, so we did not select fluoroquinolones as first-line antibiotics according to our antibiotic strategy (11). Intravenous antibiotics (cefmetazole sodium 1 g/day) were started just after admission to our hospital (Fig.…”

Kidney cyst infection through a fistula between bladder and retroperitoneal abscess in a polycystic kidney disease patient

“…1 Recent retrospective analysis suggested that the majority of cyst infections might be through hematogenous spread via bacterial translocation in the intestine with gram-negative bacteria as the most common causative organism rather than retrograde urinary tract infection. 2 Nevertheless, kidney cyst infection derived from urinary tract is still the important cause like our case derived from a transvesical fistula of retroperitoneal abscess, in which only antimicrobial treatment may not be enough and rather require the drainage of the abscess as well as the closure of the fistula to prevent continuous bacterial supply from the abscess. This case highlights the importance of identifying the infection route in the case of pyelonephritis especially in patients with ADPKD.…”

“…1 Ramucirumab is an anti-VEGFR2 antibody used to treat metastatic and/or inoperable gastric, colorectal, and non-small cell lung cancer. 2 Anti-VEGF therapies improve the survival rate of patients with advanced-stage cancers. 3 Our patient developed anti-VEGFR2 antibody-associated crescentic glomerulonephritis without thrombotic microangiopathy (TMA).…”