Diseases of the Kidney and Ureter
2.1 Acute Pyelonephritis
Ann Intern Med 1989;111:906
Cause: Gram-neg rods in 95% of cases. Most commonly Escherichia coli (particularly uropathic strains) (N Engl J Med 1985;313:44). Other responsible organisms include Klebsiella, Proteus, Enterobacter, Pseudomonas, Serratia, Citrobacter, Enterococcus faecalis, and Staphylococcus aureus. May be via ascending or hematogenous route.
Epidem: Females more than males. Increased incidence in pts with urologic instrumentation (N Engl J Med 1974;291:215), congenital urinary tract anomalies, papillary necrosis, sickle cell disease, DM, chronic indwelling catheters. Acute pyelonephritis complicates 1-2% of all pregnancies; 20-40% cases preceded by asx bacteriuria (Clin Obstet Gynecol 1984;27:17)
Pathophys: Increased bacterial resistance appears to be necessary to overcome host-resistance factors. Most cases caused by retrograde ascent of bacteria from bladder through ureter to renal pelvis and renal parenchyma. Vesicoureteral reflux (VUR), special bacterial adhesions (p. pili), and any process that interferes with nl ureteral peristalsis (obstruction, bacterial endotoxins) may facilitate bacterial ascent. Elevated renal pelvic pressure due to obstruction
or reflux enhances ascent into the collecting tubules. May be a predisposition to infections of renal medulla due to increased osmotic pressure, which causes white cell inhibition, decreased blood flow, and NH3 inhibition of C94 complement.
or reflux enhances ascent into the collecting tubules. May be a predisposition to infections of renal medulla due to increased osmotic pressure, which causes white cell inhibition, decreased blood flow, and NH3 inhibition of C94 complement.
Sx: Fever, flank pain, frequency, urgency, dysuria, hematuria, nausea
Si: CVA punch tenderness
Crs: Outpatient management in pts < 60 yr, female, not pregnant, without NV and/or dehydration, no evidence of sepsis, and without high fever. Criteria for hospitalization: male sex (underlying gu abnl common), pregnant female, temperature > 102.2°F, elevated wbc with left shift, vomiting/dehydration, evidence of sepsis, or si of inflammatory response (more than one of the following: temperature > 100.2°F or < 96.8°F, HR > 90 bpm, RR > 20, PaCO2 < 32, wbc 4000 or > 12,000 or > 10% immature bands).
Cmplc: Renal abscess, renal scarring, renal failure, HT, chronic pyelonephritis, emphysematous pyelonephritis. Children are at increased risk for scarring with pyelonephritis. Risk of premature labor is 6-50% in pregnant women with pyelonephritis (Clin Obstet Gynecol 1984;27:17).
Diff Dx: Cystitis, intercourse-induced increased bacteriuria (N Engl J Med 1978;298:321), renal abscess, acute interstitial nephritis (Ann Intern Med 1980;93:735), pelvic inflammatory disease, appendicitis, urolithiasis, biliary tract disease, acute pancreatitis, basal pneumonia
Perinephric abscess—located within Gerota’s fascia—may be cmplc of pyelonephritis or occur secondary to hematogenous spread. Two factors differentiate acute pyelonephritis from perinephric abscess: (1) pts with uncomplicated pyelonephritis often have sx 5 d prior to hospitalization, whereas those with perinephric abscess have sx longer; and (2) pts
with pyelonephritis often afebrile within 4 d of antibiotics, whereas those with perinephric abscess tend to be febrile for longer periods despite antibiotics (Medicine 1974;53:441). Renal US or CT will help localize the perinephric abscess (Urol Clin North Am 1982;9:219). Rx consists of antibiotics and drainage, either via an open approach or percutaneous drainage (Medicine 1988;67:118).
Lab: UA (microscopic), c + s from a midstream urine or catheterized urine sample. Gram stain of unspun urine shows one or more bacterium/oil immersion field. In a sx pt, urine c + s demonstrating > 102 CFU/mL is significant. Ab-coated bacteria tests are typically pos in pts with pyelonephritis. These may be neg early in disease and when humoral immune system is incompletely developed (as in an infant) and may also be pos in cystitis (Pediatrics 1979;63:467; Acta Pediatr Scand 1978;67:275).
Xray: In uncomplicated pt, studies show that imaging adds little to the management if pt responds to rx within 72 hr. If there is a role for imaging in special circumstances, CT with and without contrast most likely to provide useful information. US kidneys/bladder/retroperitoneum with KUB may be used as alternative to CT. CT may demonstrate perinephric or renal abscess or emphysema (www.guideline.gov).
Rx: Empirical outpatient treatment:
Alternatives: Cipro 400 IV × 1, then 14-d oral course
Empirical inpatient treatment
Ciprofloxacin 400 mg IV q12h: treat IV for 48 hr or after resolution of severe si, then change to oral to complete 14 d of treatment
Gentamicin/tobramycin/netilmicin 2 mg/kg loading dose IV, then 1.5-3.0 mg/kg per day as divided dose until afebrile for
48 hr or after resolution of si, then change to oral therapy to complete 14 d.
Amikacin 7.5 mg/kg IV loading dose, then 15 mg/kg per day as divided dose, then when afebrile for 48 hr change to oral therapy for 14 d.
Ampicillin/sulbactam: 1-2 g IV q6h until afebrile for 48 hr, then change to oral cephalosporins to complete 14 d of treatment.
Cefotaxime 1 or 2 g IV q8h until afebrile for 48 hr, then change to oral cephalosporin to complete 14 d of treatment.
2.2 Emphysematous Pyelonephritis
Arch Intern Med 2000;160:797-808
Cause: Acute necrotizing parenchymal and perirenal infection by gas-forming organisms. E. coli is most frequently identified organism but may also be associated with Klebsiella pneumoniae, Proteus mirabilis, Pseudomonas aeruginosa, Aerobacter aerogenes, Citrobacter, and, rarely, yeast.
Epidem: Roughly 70-90% cases involve pts with diabetes (Am J Med 1987;83:149; Diabetes Care 1989;12:229). Obstruction is main cause in pts with diabetes. May also occur in pts with urinary tract obstruction associated with calculi or papillary necrosis and significant renal impairment. Of all cases, 10% are bilateral (Urology 1985;25:293). Adults more than children; females more than males; left kidney more than right kidney.
Pathophys: Exact pathogenesis unknown, but 4 factors appear to be involved: (1) gas-forming bacteria, (2) high tissue glucose, (3) impaired tissue perfusion, and (4) defective immune response (J Urol 1994;151:125).
Huang classification of emphysematous pyelonephritis:
Class 1: gas confined to the collecting system
Class 2: gas confined to the renal parenchyma alone
Class 3A: perinephric extension of gas or abscess
Class 3B: extension of gas beyond Gerota’s fascia
Class 4: bilateral emphysematous pyelonephritis or emphysematous pyelonephritis in solitary kidney
Sx: Fever, vomiting, flank pain, urgency, frequency, dysuria, altered sensorium, shock
Si: CVA punch tenderness
Crs: Appears to be cmplc of severe pyelonephritis. There is a 43% mortality rate (J Contin Ed Urol 1979;18:9).
Cmplc: May require nephrectomy. Associated with increased mortality.
Diff Dx: Acute pyelonephritis: may have air in collecting system with acute pyelonephritis and a gas-producing bacteria; renal abscess
Xray: KUB: Intraparenchymal gas may appear as mottled gas shadows over kidney or as crescentic collection of gas over upper pole of kidney. Gas may be identified in perinephric space or retroperitoneum. IVP not helpful because affected kidney is poorly functioning. US may show strong focal echoes that suggest intraparenchymal gas (Am J Radiol 1979;132:656; 1979;132:395). CT scan is the definitive test.
Rx: Initial rx is fluid resuscitation, antibiotics, and relief of obstruction, if present (BMC Nephrol 2002;3:4). If no improvement, then surgical or percutaneous drainage or nephrectomy (J Urol 1997;157:1569). High mortality rate of 19-40%. Class 1 and 2 can be managed with percutaneous drainage and antibiotics; class 3 and 4 in presence of 2 or more risk factors (thrombocytopenia, increased serum creatinine, altered sensorium, shock), nephrectomy yields better results.
2.3 Renal Abscess
Cause: Prior to antibiotic era, 80% of renal abscesses were attributed to hematogenous seeding by Staphylococcus (Surg Gynecol Obstet 1930;51:654). Currently, gram-neg organisms are the most common cause of adult abscesses, usually via retrograde ascent (renal corticomedullary abscess.
Epidem: E. coli responsible for 75%. DM (47%), renal calculi (41%), and ureteral obstruction (20%) are the most common predisposing factors to abscess (Am J Emerg Med 1999;17:192). Association between VUR and renal abscess rarely noted (J Urol 1973; 109:1029). Recurrent UTIs are risk factor.
Pathophys: Complicated UTI associated with stasis, calculi, malignancy, neurogenic bladder, and DM appear to predispose to abscess formation (Urology 1980;16:333). Most commonly related to ascending infection associated with tubular obstruction from prior infections or calculi.
Sx: Fever, chills, malaise, urgency, frequency, dysuria
Si: Abdominal or flank pain and weight loss
Crs: Often there is a delay in diagnosis; only 15-25% of pts reported to be diagnosed at time of admission (Urology 1980;16:333). Prognostic factors that may affect morbidity and mortality include older age, lethargy, and increased BUN as poor outcome predictors (Am J Emerg Med 1999;17:192). Renal and perinephric abscesses caused by S. aureus respond better to antibiotics than gram-neg abscesses (West J Med 1982;136:95).
Size of abscess affects the likelihood of resolution with antibiotics alone. Factors that predict a less favorable outcome to antibiotic therapy alone include abscess diameter > 3-5 cm, involvement with more than 1 organism, presence of gram-neg bacilli, duration of treatment longer than 4 wk, and use of aminoglycoside as the only antibiotic (J Urol 1996;155:52; Clin Infect Dis 1996;231:592).
Cmplc: Sepsis, loss of renal function, perinephric abscess, mortality rate of 1.5-15%
Diff Dx: Pyelonephritis, renal tumor
Lab: CBC demonstrates marked leukocytosis; blood cultures usually positive. UA; c + s often pos, but may be neg in setting of hematogenous spread; BUN and creatinine often increased
Xray: Xray findings depend on nature and duration of infection. CT scan is most accurate method of staging renal infections (Radiology 1994;192:297). CT and US permit 82-90% accuracy in dx of renal abscess (Urol Clin North Am 1987;14:91). Initially, CT may show renal enlargement and focal, rounded areas of decreased attenuation. After several days, there may be a thick fibrotic wall around the abscess. Chronic abscess reveals obliteration of tissue planes, thickening of Gerota’s fascia, and low-attenuation parenchymal mass surrounded by an inflammatory wall of slightly higher attenuation that enhances with contrast due to the increased vascularity of the abscess wall (Urol Clin North Am 1983; 9:185; Radiology 1979;13:171).
Rx: Traditional rx is open or percutaneous drainage and antibiotics (Urology 1985;25:142; J Urol 1982;127:425). Stable immunocompetent pts with renal abscesses < 3 cm may be treated with 6 wk of IV antibiotics (J Urol 1996;155:52). Empirical treatment pending culture results may include piperacillin and tazobactam (Zosyn), ticarcillin and clavulanate (Timentin), Nafcillin (Nafcil) if suspect Pen G-resistant staph or strep, amikacin, gentamicin, tobramycin, ciprofloxacin, ceftazidime (Fortaz), cefepime (Maxipime).
2.4 Renal and Ureteral Tuberculosis
Cause: Mycobacterium tuberculosis, blood-borne mets. Previous lung infection may occur many years before renal/ureteral disease. Rarely may be secondary to bacillus Calmette-Guérin (BCG) therapy (Urologia Internationalis 2004;72:257).
Epidem: Prevalence rate 5% in Western world and 1-3% in Nigeria (West African J Med 2001;20:217). Male-to-female ratio is 2: 1; most pts 20-40 yr, but increased incidence among pts 45-55 yr and among pts > 70 yr. Autopsy study of pulmonary tuberculosis (TB) revealed unsuspected renal foci in 73% cases, usually bilateral (Am Rev Resp Dis 1975;111:647). Most common site of ureteral involvement is distal ureter at ureterovesical junction (UVJ). Renal TB is the most common form of extrapulmonary TB among whites (West African J Med 2001;20:217). Ureteral involvement present in 50% pts with gu TB (Radiol Clin North Am 1995;33:691).
Pathophys: Blood-borne. Bacteria settle in blood vessels, typically near glomeruli. Depending on dose of infecting organism, virulence of organism, and host resistance, tubercles may be replaced by fibrous tissue or continue to multiply and coalesce, leading to caseous necrosis.
Sx: Flank pain if obstructed
Crs: May lead to calyceal strictures, calyceal destruction, ureteropelvic junction obstruction (UPJO), TB interstitial nephritis, abscess formation, and ureteral strictures, more often multiple and located in distal 1/3 of ureter (Radiol Clin North Am 1995;33:691).
Lab: UA, c + s sterile pyuria (typically, 20 wbc/hpf) common, but superimposed infection is present in 20% (Campbell’s Urology 1998; 7:807). Microscopic hematuria and intermittent gross hematuria may occur. Culture of 3 morning urine specimens for mycobacteria establishes dx in 80-90% of cases (Principles and Practice of Infectious Disease 2000;5:2602). PPD: A positive reaction indicates that pt has been infected, provided pt has not been vaccinated with BCG, but it can’t be regarded as indication of active TB. PCR sens 87-100% and specif 92-99%, with results available in approx 6 hr (Urology 2000;56:570-574)
Xray: KUB may show calcification in areas of kidney or lower urinary tract in 50%. CT more sensitive in detecting calcifications, TB within collecting system characterized by thick wall and fibrosis on CT. Various sites of hydro can be demonstrated on CT depending on sites of strictures (J Comput Assist Tomogr 1997;21:254).
Rx: Antibiotics: Standard therapy is rifampin, INH, pyrazinamide, and ethambutol for 2 mo, then rifampin and INH for 4 more mo unless resistance to either agent exists; in HIV pts, treat for 9 mo. Steroids indicated if severe bladder sx and/or ureteral involvement. Pts should be followed regularly after chemotherapy at 3, 6, 9, and 12 mo with urine culture and IVP. If small calcifications present, then yearly KUB to follow the size of these. Surgical intervention indicated for large calcifications, nonfunctioning kidney with extensive calcification, and stricture disease (J Urol 1980;124:187; 1980;123:822).
2.5 Xanthogranulomatous Pyelonephritis
Cause: Rare, severe, chronic renal infection that typically results in diffuse destruction of the renal tissue. Occurs in setting of obstruction and infection. Proteus is most common organism.
Epidem: Most cases are unilateral. Found in 0.6-1.4% pts with renal inflammation evaluated pathologically (BJU 1972;44:296; Am J Clin Pathol 1955;25:1043). Peak incidence is sixth and seventh decades, but may occur in children also (J Urol 1974;119:589; Eur J Pediatr Surg 2002;2:42). Females more than males; 15% have DM.
Pathophys: Thought to start with obstruction (stone or sloughed papilla) followed by infection that leads to destruction of tissue and deposition of lipid material by histiocytes. Granulomatous process then occurs. Xanthoma cells: lipid-laden macrophages. May affect kidney alone or progress to involve perinephric fat and retroperitoneum.
Sx: Flank tenderness, malaise, urgency, dysuria
Si: Fever, chills, flank pain, palpable flank mass, frequency
Crs: May be treated with drainage, but may progress to involve entire kidney, requiring nephrectomy
Cmplc: Renal cell carcinoma (RCC), transitional cell carcinoma (TCC) (see 2.19 and 2.22, respectively), and squamous cell carcinoma of the pelvis have occurred with xanthogranulomatous pyelonephritis (XGP) (J Urol 1981;125:398; 1981;126:437; 1980; 124:125).
Diff Dx: Renal mass
Lab: UA, c + s; CBC may demonstrate anemia; hepatic dysfunction in up to 50% of pts (J Urol 1978;119:589).
Xray: US: no specific ultrasonographic features that allow for distinction of focal XGP from renal tumors or abscesses (J Ultrasound Med 2004;23:409). CT is imaging technique of choice and allows for determination of extent of disease; low-density fluid-filled areas within the renal parenchyma and findings indicating perinephric extension are suggestive of XGP (Scand J Urol Nephrol 2003;37:342).
Rx: If cannot r/o malignancy, nephrectomy is indicated. Often performed open; however, in skilled hands and with limited disease, may be performed via a hand-assisted laparoscopic approach (J Endourol 2004;18:770). If drainage is attempted first, must watch closely as condition may continue and may develop into a renal-cutaneous fistula.
2.6 Malacoplakia
Cause: Exact etiology unknown. Condition appears to be related to abnl intracellular killing by phagocytes, particularly macrophages.
Localized to gu tract (58% of cases), bladder (40%), prostate, kidney (16%), ureter (11%), renal pelvis (10%), and testes. May be noted in other sites, including skin, vulva, vagina, adrenal, cerebrum, lungs, vertebrae, endometrium, pleura, gluteal muscles, tonsils, conjunctiva, spleen, hip joint (J Urol 1981;125:139).
Localized to gu tract (58% of cases), bladder (40%), prostate, kidney (16%), ureter (11%), renal pelvis (10%), and testes. May be noted in other sites, including skin, vulva, vagina, adrenal, cerebrum, lungs, vertebrae, endometrium, pleura, gluteal muscles, tonsils, conjunctiva, spleen, hip joint (J Urol 1981;125:139).
Epidem: Female-to-male ratio of 4:1. Peak incidence is > 50 yr (BJU 1982;54:181). Most pts (80-90%) have persistent UTI; E. coli is most commonly identified organism (70%) (J Pathol 1983;140: 275; J Urol 1981;125:139). Some pts (40%) have intercurrent systemic illness, carcinoma, AIDS, or autoimmune disease (Urol Radiol 1990;12:157). Bilateral renal involvement in 64% of pts with renal disease.
Pathophys: Thought to be related to defective lysosomes and abnl microtubular assembly. May reflect alterations in cGMP and AMP levels (BJU 1999;84:464). Pathognomonic dx of malacoplakia are intracytoplasmic and extracytoplasmic inclusions, Michaelis-Gutman bodies. Calcium phosphate crystals and iron are main components of the Michaelis-Gutman body. Dx confirmed by histopathology.
Sx: Bladder (frequency, urgency, dysuria), prostate (obstructive voiding sx), and renal (flank pain, NV, abdominal pain)
Si: Prostate (firm, enlarged prostate, elevated PSA), renal (fever, palpable mass), testes (palpable intratesticular mass); 70% are fluctuant (Am J Clin Pathol 1967;47:135).
Crs: If untreated, may progress to large fungating mass; if in ureter, may lead to obstruction and loss of renal function.
Cmplc: Mortality can exceed 50% (J Urol 198;125:139). Bilateral renal involvement is uniformly fatal (J Urol 1992;147:115).
Diff Dx: Renal (megalocystic interstitial nephritis, xanthogranulomatous pyelonephritis, lymphoma, amyloidosis, pyelonephritis, glomerulonephritis, vasculitis, renal vein thrombosis); bladder (bladder cancer); prostate (prostate cancer); ureter (ureteritis cystica)
Lab: UA: Hematuria, pyuria, bacteriuria. Urine culture. CBC: anemia present in 82% of cases, elevated wbc in 60% (Am J Kidney Dis 193;22:243). Increased PSA may be present with prostatic involvement.
Xray:
Renal disease: US demonstrates multiple irregular masses, renal enlargement, distorted echogenicity (J Urol 1992;147: 115; Br J Radiol 1985;58:175; 1984;57:751). CT demonstrates poor enhancement, lack of excretion, renal enlargement, multiple mildly enhancing heterogeneous solid masses (J Urol 1992;147:115; Am J Nephrol 1990;10:416; Radiology 1980;136:33).
Bladder: CT demonstrates circumferential bladder wall thickening, multiple lobules, large masses (J Compute Assist Tomogr 1985;9:119; 1983;7:541).
Rx: Mainstay of rx is long-term antibiotics. Quinolones effective in 80-90% of pts. Other agents, such as Tm/S, which assist intracellular killing of bacteria, may be used. In select studies, vitamin C and bethanechol have been helpful in controlling the disease by increasing cGMP-to-cAMP ratio, which improves macrophage function (J Urol 1979; 122:703; N Engl J Med 1977;279:1413). Renal-percutaneous bx may be helpful in establishing dx (Br J Radiol 1998;71:1083). For unilateral disease, nephrectomy leads to 90% cure rate (Arch Intern Med 1996;156:577): testis—orchiectomy and antibiotics; prostate—confirm disease with prostate bx, treat with antibiotics and vitamin C for up to 6 mo. If PSA elevated, expect it to decrease with effective rx. Bladder—TUR of lesion in addition to antibiotics; ureter—successful rx with stenting and antibiotics reported (BJU Int 1987;59:485).
In immunocompromised pts with malacoplakia, discontinue or taper immunosuppressive therapy whenever possible.
2.12 Retroperitoneal Fibrosis
Cause: Proposed causes include retroperitoneal hemorrhage, urinary extravasation, trauma, perianeurysmal inflammation, radiation therapy, surgery, inflammatory bowel disease, collagen disease, fat necrosis, malignancy, infections, methysergide (Sansert) induced (BMJ 1988;296:240; Can J Surg 1984;27:111; Surgery 1977;81: 250) and rarely associated with Reidel’s thyroiditis (BMJ 1988; 296:240; Can J Surg 1984;27:111; Surgery 1977;81:250).
Epidem: Incidence is 1 in 200,000 (J Urol 1996;156:1403). Male-to-female ratio of 2:1 to 3:1, peak incidence between 40 and 60 yr (J Urol 1979; 122:1). Uncommon in childhood. Classified into 2 groups: idiopathic (2/3 of cases) and secondary. Retroperitoneal
fibrosis associated with cancer, drugs, chemical products, infections, inflammatory diagnoses, retroperitoneal bleeding, or radiotherapy.
fibrosis associated with cancer, drugs, chemical products, infections, inflammatory diagnoses, retroperitoneal bleeding, or radiotherapy.
Table 2.1 Aspergillosis, Blastomycosis, Coccidiomycosis, Cryptococcus, Histoplasmosis | ||||||||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
