Diversity and Complexity of Urinary Tract Infection in Diabetes Mellitus

Lukman M. Hakeem, Diptendu N. Bhattacharyya, Cyril Lafong, Khalid S. Janjua, Jonathan T. Serhan and Ian W. Campbell


British Journal of Diabetes and Vascular Disease. 2009;9(3):119-125. 

In This Article


There are several reasons for an increased frequency of UTIs in diabetic patients. Several aspects of immunity are altered in patients with diabetes. Polymorphonuclear leukocyte function is depressed, particularly when acidosis is present. Leukocyte adherence, chemotaxis, and phagocytosis may be affected.[21,22,23] Antioxidant systems involved in bactericidal activity may also be impaired.[24] A lower urinary concentration of cytokines (IL8 and IL6) has been shown to correlate with a lower urinary leukocyte cell count in diabetic patients, which may contribute to the increased incidence of UTIs in this patient group.[25,26] Other factors may also be involved. Poor glycaemic control, and the resulting hyperglycaemia, by itself does not predict increased bacterial rates of multiplication and has not always been shown to be a major determinant of either the incidence of bacteriuria or its subsequent complications.[27,28,29]

Increased adherence E. coli expressing type-1 fimbriae (a virulence factor) to uroepithelial cells of diabetic women may play an important role in the pathogenesis of UTI, especially if diabetes is poorly controlled.[30] Tamm–Horsfall protein, which traps type 1 fimbriated E. coli in uromucoid present on epithelial cells, acts as an important defence mechanism as it prevents adherence and cell entry of pathogens. This protein is significantly reduced in some patients with diabetes.[31,32] Micturation abnormalities secondary to diabetic neuropathy occur in 10–40% of patients with longstanding diabetes resulting in increased residual urine. This presumably accounts for some of the increased morbidity and increased susceptibility to infection.[33]

Emphysematous complications in renal tissue are likely to be due to the presence of organisms that rapidly ferment glucose and produce carbon dioxide. Impaired transport of metabolic end products either due to impaired tissue perfusion or some other factor in diabetes may also contribute.[16,34] Pathogenesis of acute papillary necrosis is not well understood. It is presumed to be due to a marginal change in vascular supply, which is further stressed by infection leading to infarction and sloughing of papillae.[17]

Renal cortical abscess results from haematogenous spread of bacteria from a primary extrarenal focus of infection. In contrast, renal corticomedullary abscess develops as an ascending infection. Severe renal parenchymal involvement in combination with corticomedullary abscess is more likely to extend to the renal capsule and perforate, thus forming a perinephric abscesses (figure 2).

Figure 2.

Contrast enhanced CT of abdomen showing large right-sided perinephric collection containing fluid and gas in a 70-year-old woman with type 2 diabetes and a history of renal calculi admitted with right renal angle tenderness and fever, 2 weeks after lithotripsy and ureteric stenting. The patient had been commenced on ciprofloxacin 500 mg twice daily when she had developed fever after the procedure. Mid-stream urine isolated enterococci. The patient was commenced on piperacillin/tazobactam 4.5 g three times and transferred to the urologist where she underwent ultrasound guided percutaneous drainage of the abscess