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Home , Glycosuria

CASE REPORT

Transient in a Patient with Acute Pyelonephritis Chung-Jung Wu

Abstract Case Report Glycosuria was detected in a 37-year-old Chinese woman Weencountered a 37-year-old Chinese womanwhohad by a urinary examination in a local clinic with clinical evi- spiking fever up to 40.0°C and knocking tenderness over the dence of acute pyelonephritis (APN). Transient glycosuria right costophrenic angle for 2 days. She was transferred to our is an unusual complication of acute pyelonephritis in non- hospital immediately under the suspicion of fresh diabetic case diabetic patients. As there is growing prevalence of type 2 with right side APNdue to the urinary finding of glycosuria in the population worldwide, it must be recognized and (2+ , 1+ protein, 2+ glycosuria, 2+ oc- that mistaken diagnosis of diabetes mellitus by glycosuria cult blood). At our hospital, a Chemstrip urinalysis was per- maypredispose patients to an unfavorable hypoglycemic formed and demonstrated the presence of 1+ pyuria, 1+ hema- episode. Thus definite diagnosis of diabetes mellitus should turia, and 4+ of glycosuria. The simultaneous postprandial blood be madeonly after recovery ofAPNby means of urinalysis concentration was 137 mg/dl (Table 1). During hospi- or by simultaneous blood glucose concentration analysis. talization, sonography and CTscan of the kidneys were per- (Internal Medicine 40: 519-521, 2001) formed and their findings were compatible with the diagnosis ofAPNover right , without evidence of obstructive neph- Key words: blood glucose, glucose tolerance test, diabetes ropathy. and blood cultures yielded colonies of Escheri- mellitus, fever chia coli later. Empirical antibiotics (cephalosporin and gen- tamicin) were prescribed in addition to intravenous hydration. Spiking fever subsided at 72 hours later and her symptoms improved also. Fasting blood glucose levels were followed Introduction during hospitalization (99 mg/dl after fever subsided for 3 days, at 7th hospital day) and 1-2 weeks after discharge (83 mg/dl; Normalurine contains small amounts of glucose, called basal simultaneously urinalysis showed negative glycosuria) and all glycosuria, whichis undetectable under normalconditions. The levels were within the normal range (Table 1). renal threshold for glucose excretion in healthy adults corre- She was admitted again 1-2 months later with recurrent APN. sponds to a plasma glucose concentration of about 1 80 mg/dl. But there was no glycosuria found during this second hospital- Most healthy, non-diabetic individuals do not present glyco- ization and her fever subsided within 24 hours under the therapy suria except some individuals, such as children and pregnant of empirical antibiotics. women,whomaypresent very low or variable renal threshold, The 75-g oral glucose tolerance test (OGTT) was performed leading to glycosuria in euglycemia (1). Acute pyelonephritis a few months later in ambulant status (Table 2). The overnight (APN) has rarely been implicated as the causative etiology of fasting urinalysis showed essentially normal and negative gly- renal glycosuria in adults and standard textbooks do not in- cosuria. The result of OGTT(fasting blood glucose of 87 mg/ clude APNin the differential diagnosis of renal glycosuria. The dl and 2-hour post-OGTT blood glucose of 138 mg/dl) did not association of transient renal glycosuria and APNwas first re- put the patient in the diagnostic category of diabetes mellitus ported in 1989 in the English literature when Trachtman and according to the 1997 ADAcriteria (3) (all fasting blood glu- Kahn (2) reported a 9-month baby girl with APNand renal cose less than 100 mg/dl) and 1998 WHOcriteria (4) for a glycosuria. Since then, there has been no English literature diagnosis of diabetes mellitus. Also there was no resis- implicating APNas the cause of adult glycosuria. tance status found during the glucose tolerance test.

From Division of and Metabolism of Internal Medicine, Chia-Yi Veterans Hospital, Chia-Yi, Taiwan, ROC Received for publication August 14, 2000; Accepted for publication November 23, 2000 Reprint requests should be addressed to Dr. Chung-Jung Wu, Division of Endocrinology and Metabolism of Internal Medicine, Chia-Yi Veterans Hospital, No. 600, Section 2, Ssu-Hsien Road, Chia-Yi 60093, Taiwan, ROC

Internal Medicine Vol. 40, No. 6 (June 2001 ) 519 Wu

Table 1. Time Courses of Simultaneous Fasting Blood Glucose (FBG) Levels and Uri- nalysis Results 1stday 4thday 7th day ll days afterdischarge Fever pattern Fever, spiking No fever FBG 137 mg/dl* 99 mg/dl 83 mg/dl Urinalysis Color Yellow Yellow App. Clear Cl ear Specific gravity 1.010 1.01 5 pH 8.0 6.5 Nitrite test (-) (-) Protei n (±) (-) Glucose (4+) (-) Ketone (-) (-) WB C (+) (-) RB C (+) (-) B acteri a (+) (-) *Random, non-fasting, blood glucose level during episode of acute pyelonephritis.

random blood glucose). It is possible that heavy glycosuria may Table 2. 75-g Oral Glucose Tolerance Test (OGTT)* lead us to speculate the possibility of underlying diabetes mel- Blood glucose level Serum insulin level litus, especially during acute medical condition as in the present case. But a definite diagnosis of diabetes mellitus should be Before OGTT madeonly after recovery of APNby meansof urinalysis or 1 hour after OGTT simultaneous blood glucose concentration analysis. Wemust 87 mg/dl 225 mg/dl 138 mg/dl 5.0 juIU/ml 80.9 MlU/ml 2 hours after OGTT 40. 1 |iIU/ml keep in mind that patients with type 2 diabetes face a chronic, progressive disease that leads to complications that profoundly *OGTTwas performed in stable condition and it shows no diagnostic affect both quality of life and longevity. The diagnosis of dia- result in addition to normal urinalysis. betes mellitus maybe a heavy psychological burden to patients. The etiology of renal glycosuria may be genetically deter- mined as , but there are some factors associ- Discussion ated with renal glycosuria, as ACEinhibitor usage (8), in neph- rotic syndrome (9), with ethanol consumption (10), in patients Glycosuria maybe due to in the presence of with tetanus (1 1), arsenic exposure (12) and so on. The present normal renal glucose handling (hyperglycemic glycosuria) or case did not have aforementioned medication or associated to abnormalities of tubular glucose transport at normal blood condition and it should be attributed to the course ofAPN. glucose concentrations (renal glycosuria). Renal glycosuria is During the period of active APN, marked stress such as high often a benign condition whosemajor clinical significance is fever or resultant insulin resistant state mayincrease the blood to distinguish it from other moreserious causes of glycosuria, glucose levels, although within the non-diabetic range, which the most important of which is diabetes mellitus. Self-moni- mayoccasionally cause transient glycosuria. But the glyco- toring of glycosuria is more appropriate in out-clinics and in suria, if present, is usually mild in non-diabetic patients, un- patients with diabetes mellitus as it is relatively cheap, easy to like the marked glycosuria in the present case. Also glycosuria use, and less painful when compared to blood glu- may become positive (as renal glycosuria) in non-diabetic pa- cose monitoring (5). tients just because of lowering the renal threshold for glucose, However, the experience in this case indicates that caution especially during inflammatory renal disease that disturbs re- is neededin the application of heavyglycosuria as a diagnostic nal tubular function or during a condition associated with fe- marker for diabetes mellitus, as a mistaken diagnosis mayput ver process via unknowncytokines or mediators. But this topic patients at risk of hypoglycemia due to diabetic treatment (6). is still unsolved. Most patients with APNdo not develop renal glycosuria, but It has been found that levels of IL-loc, IL-6 and IL-8 are transient glycosuria can occur as an unusual complication. As markedly increased in the urine of patients with acute pyelo- diabetes mellitus is still diagnosed as a first test via urinalysis nephritis ( 1 3, 14), and that Escherichia coli pyelonephritis may by physicians in some countries, for example, about 13%in contribute to the expression ofTGF-p(15). But there is still no US (in Pittsburgh, Pennsylvania in the early 1990's) reported detailed knowledge of biological events in the process of tran- by Stolk et al (7) (64% via fasting plasma glucose and 28% via sient glycosuria associated with APNand what role renal tu-

520 Internal Medicine Vol. 40, No. 6 (June 2001) Renal Glycosuria in Acute Pyelonephritis

5) Gallichan M. Self-monitoring of glucose by people with diabetes: Evi- bular dysfunction or diminished renal threshold for glucose dence based practice. BMJ 314: 964-967, 1997. play. Rezaian et al (1 1) report that glycosuria in patients with 6) Orem J, Mpanga L, Habyara E, Nambuya AM, Otim MA. Renal glyco- tetanus is possibly induced by tetanospasmin. The possible suria treated as diabetes mellitus: Case report. East Afr MedJ 74: 740- explanations in our case maybe that somestrain of bacterial 742, 1997. infection or its toxins, in a genetically predisposed individual, 7) Stolk RP, Orchard TJ, Grobbee DE. Whyuse the oral glucose tolerance mayplay a role in the development of transient glycosuria in test? Diabetes Care 18: 1045-1049, 1995. 8) Milavetz JJ, Popovtzer MM.Angiotensin-converting enzyme inhibitors APN, possibly via lowering renal threshold for glucose by toxin- and glycosuria. Arch Intern Med 152: 1081-1083, 1992. or cytokine-mediated renal tubular dysfunction. In summary, 9) Reubi FC, Seiler A. Renal glycosuria in patients with the nephrotic syn- transient glycosuria maybe an unusual complication of acute drome. Klin Wochenschr 62: 621-630, 1984. pyelonephritis, and it should not be regarded as a marker of 10) Ito S, Ueno M, Izumi T, Arakawa M. Induction of transient , , and glycosuria by ethanol consumption in Japanese alcohol- diabetic diagnosis unless it is associated with simultaneously ics. 82: 246-253, 1999. marked hyperglycemia. 1 1) Rezaian GR, Khajehdehi P, Beheshti S. Transient renal glycosuria in pa- tients with tetanus. Nephron 80: 292-295, 1998. References 12) Rahman M, Tondel M, Chowdhury IA, Axelson O. Relations between exposure to arsenic, skin lesions, and glycosuria. OccupEnviron Med56: 1) Mogensen CE, Osterby R, Gundersen HJ. Early functional and morpho- 277-281, 1999. logical vascular renal consequences of the diabetic state. Diabetologia 13) Roberts JA, Roth JK Jr, Domingue G, Lewis RW, Kaack B, Baskin G. 17: 71-76, 1979. Immunology of pyelonephritis in the primate model. V. Effect of super- 2) Trachtman H, Kahn R. Renal glycosuria in pyelonephritis. Pediatrics 83: oxide dismutase. J Urol 128: 1394-1400, 1982. 652-653, 1 989 (letter). 14) Tullus K, Fituri O, Burman LG, Wretlind B, BraunerA. Interleukin-6 and 3) Report of the Expert Committee on the Diagnosis and Classification of interleukin-8 in the urine of children with acute pyelonephritis. Pediatr Diabetes Mellitus. Diabetes Care 20: 1 183-1 197, 1997. Nephrol 8: 280-284, 1994. 4) Alberti KG, Zimmet PZ. Definition, diagnosis and classification of dia- 15) Pimentel JL Jr, Sundell CL, Wang S, Kopp JB, Montero A, Martinez- betes mellitus and its complications. Part 1 : Diagnosis and classification MaldonadoM. Role of angiotensin II in the expression and regulation of of diabetes mellitus provisional report of a WHOconsultation. Diabet transforming growth factor beta in obstructive nephropathy. Kidney Int Med 15: 539-553, 1998. 48: 1233-1246, 1995.

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