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Sumário de Urina
This document summarizes key aspects of urine analysis: - Urine dipstick tests can detect pH, density, glucose, ketones, leukocyte esterase, blood, protein, nitrites, and urobilinogen. Microscopic sediment examination identifies red blood cells, white blood cells, bacteria, crystals, and casts. - Various types of casts like waxy casts, granular casts and hyaline casts indicate different types of kidney damage. Crystals seen can indicate ethylene glycol or indinavir toxicity. - Hematuria workup involves urine dipstick, microscopy and cystoscopy depending on risk factors. Findings like acanthocytes suggest glomerular causes while others suggest
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Sumário de Urina
- 1. Sumário de UrinaPaulo Novis Rocha ( [email_address] ) Professor Adjunto do Depto de Medicina Faculdade de Medicina da Bahia - 200 anos
- 2. Exame da Urina:Exame laboratorial mais antigo!
- 3. História Papiros egípcios400 AC - Hipócrates Século I, Caraka, 10 tipos de urina Século II, Galeno, teoria dos humores Século X, Isaac Judaeus, uromancia, 20 tipos de urina Século XVII, microscópio, sedimento urinário Século XIX, Addis Un disco de vidrio de orina con 20 matices de color (1491 DC)
- 4. Exame da urinaConstitui um dos meios mais simples e seguros para se comprovar a patologia intrínseca do trato urinário. Componentes: Aspecto Fita reagente (Dipstick) Análise do sedimento
- 5. Fita reagente (dipstick) pH Densidade Glicose Cetonas Esterase leucocitária Sangue Proteína Nitrito Urobilinogênio
- 6. Dipstick : pHVaria normalmente de 4,5 a 7,8 Não constitui, isoladamente, índice da capacidade excretora de íons H + Utilidades: ITU Acidose tubular renal distal Urolitíase Comprovar alcalinização da urina em certas situações
- 7. Dipstick : densidadeVaria normalmente entre 1.002 e 1.032 Substitui grosseiramente a osmolaridade Utilidades: estado de hidratação capacidade de concentração urinária interpretação de outros componentes do sumário de urina
- 8. Dipstick : glicoseDetecção de glicosúria Utilidades: Diagnóstico e controle do diabetes mellitus Determinação de distúrbio tubular proximal Glicosúria renal, síndrome de Fanconi
- 9. Dipstick : CetonasDetecção de cetonúria Cetose de jejum, cetoacidose diabética Sensível ao ácido aceto-acético, porém não acusa o beta-hidroxibutírico
- 10.
- 11. Dipstick : esteraseleucocitária Detecção de piúria Exame do sedimento, colorações Diagnósticos: ITU Tuberculose renal Nefrite intersticial Glomerulonefrites
- 12. Dipstick : sangueDetecção de hematúria Importante confirmar presença de hemácias no sedimento Na ausência de hemácias: hemoglobinúria mioglobinúria
- 13. Dipstick : proteinúriaImportante para diagnóstico diferencial da etiologia da doença renal Só detecta albumina Exame da tira reagente é meramente qualitativo Quantificação exige urina de 24 horas ou razão proteína/creatinina urinária
- 14.
- 15. Proteinúria: significado clínico“ Funcionais” Estados patológicos diversos Infecções urinárias Doença renal glomerular vs não glomerular 150 mg, 1000 mg, 3500 mg
- 16. Análise do Sedimento:A biópsia renal do pobre Hemácias Leucócitos Bactérias Cilindros Cristais
- 17.
- 18. Urine dipstick +Repeat Urine dipstick Workup ends Microscopic analysis Myoglobin Hemoglobin Workup ends Cystoscopy Cystoscopy > 50 years old or risk factors for bladder Ca < 50 years old, no risk factors for bladder Ca Isomorphic red cells NON-GLOMERULAR Referral Helical CT Urine cytology - - + + - + - Acantocytes, casts GLOMERULAR Isolated Microhematuria Proteinuria, renal failure Routine checkup Referral
- 19. Hematúria Phase contrastmicroscopy
- 20.
- 21. Urine from a34-year-old man with biopsy-proven IgA nephropathy
- 22. Cilindros Formações alongadase de contorno regular Originam-se ao nível dos túbulos distais ou ductos coletores Todos se organizam às expensas da mucoproteína de Tamm-Horsfall
- 23. NTA, nefrite intersticialCélulas tubulares Pielonefrite, nefrite intersticial Leucocitário Glomerulonefrite Hemáticos Urina concentrada, estados febris, exercício, diuréticos (não é = doença renal) Hialinos NTA; não-específico Granulares Doença renal crônica Céreos largos Significado Tipo de Cilindro
- 24.
- 25. “ Futuro CilindroHemático” na Biópsia Renal
- 26.
- 27. Panel A showsred-cell cast (arrow) Panel B shows dysmorphic red cells (arrows)
- 28. In Panel A(x 440), urinary sediment shows a red-cell cast and red cells In Panel B (x 440), urinary sediment shows normal red cells (arrow) and crenated red-cell forms with spicules (arrowhead). Crenated red cells form in concentrated urine and are not diagnostically relevant. In Panel C (x 440), a more specific finding of glomerular bleeding is shown. Acanthocytes are doughnut like cells with membrane blebs attached .
- 29. IgA Nephropathy PANELA PANEL B Moderate mesangial matrix expansion, mild hypercellularity Mesangial IgA deposition
- 30.
- 31. Urine dipstick +Repeat Urine dipstick Workup ends Microscopic analysis Myoglobin Hemoglobin Workup ends Cystoscopy Cystoscopy > 50 years old or risk factors for bladder Ca < 50 years old, no risk factors for bladder Ca Isomorphic red cells NON-GLOMERULAR Referral Helical CT Urine cytology - - + + - + - Acantocytes, casts GLOMERULAR Isolated Microhematuria Proteinuria, renal failure Routine checkup Referral
- 32. Cilindro eritrocitárioCilindro hemoglobina hemácias
- 33. Poststreptococcal GN Marked,diffuse hypercellularity, with infiltration of PMNs Large, nodular, subepithelial deposits referred to as "humps" PANEL A PANEL B
- 34. Anti-GBM Disease PANELA PANEL B Large crescent and compressed glomerular capillary tufts Linear deposition of IgG along the GBM
- 35. Urine dipstick +Repeat Urine dipstick Workup ends Microscopic analysis Myoglobin Hemoglobin Workup ends Cystoscopy Cystoscopy > 50 years old or risk factors for bladder Ca < 50 years old, no risk factors for bladder Ca Isomorphic red cells NON-GLOMERULAR Referral Helical CT Urine cytology - - + + - + - Acantocytes, casts GLOMERULAR Isolated Microhematuria Proteinuria, renal failure Routine checkup Referral
- 36.
- 37.
- 38. Cilindro leucocitárioBactérias
- 39.
- 40. Lipóide birrefringente Cilindro hialino Corpo graxo ovalado Cilindro epitelial Cilindro céreo Cilindro graxo
- 41. Cilindros Graxo Polarizedlight microscopy
- 42.
- 43. Cilindros Granulares naNTA Klahr et al., NEJM 1998, 338 (10):671-675
- 44.
- 45. A 26-year-old manhad sudden fever and chills with severe muscle pain and weakness in his legs and pectoral muscles while mountaineering in the Andes. He was brought to a local hospital, where he received hemodialysis three times because of anuria and a rapid rise in the serum creatinine level before being transferred to our unit.
- 46. The following laboratoryvalues were recorded on admission to our unit: Urine dipstick analysis was positive (+++) for protein and blood. Myoglobin 283 µg/dl Phos 6.19 mg/dl Ca++ 8.16 mg/dl CK 1990 U/l BUN 85 mg/dl Cr 10.5 mg/dl
- 47. Myoglobinuria Sedimento urinárioBiópsia renal
- 48. Possible causes ofthe rhabdomyolysis were physical strain at high altitude and the consumption of coca leaves and coca tea to prevent mountain sickness. No infectious cause could be identified. The patient had anuria or oliguria for 10 days. He received a total of seven sessions of hemodiafiltration, until urine flow returned and the serum creatinine levels began to fall. At the time of discharge, he had a serum creatinine level of 1.0 mg per deciliter.
- 49.
- 50. Waxy casts have a smooth consistency but are more refractile and therefore easier to see compared to hyaline casts. They commonly have squared off ends, as if brittle and easily broken Waxy casts indicate tubular injury of a more chronic nature than granular or cellular casts and are always of pathologic significance
- 51.
- 52. Unresponsive at 18The patient is a 18 year old male presenting to the ED by paramedics after found at home unresponsive, face down in bed. According to friends, the patient had consumed several beers and wine earlier that day following a period of depression. The patient was orally intubated in the field by paramedics after no response to D50 and naloxone administration .
- 53. Physical Exam: General:Patient responsive only to deep painful stimuli Vitals: BP 150/70, HR=92, RR=24, T=95.4F Lungs: CTA, BS Equal, (Intubated) CV: RRR, no murmur Abd: Soft, Non-Tender, No Trauma, No Masses Rectal: Normal Tone, Heme- Neuro: DTR's Hyporeflexive, Withdraws to Painful Stimuli
- 54. Diagnostic Studies CBC:WBC 29K HCT=45 ABG: 6.97 PO2=321 PCO2=15 Lytes: Na=145 Cl=105 K=5.2 HCO3=5 BUN/Cr: 28/1.8 Glucose 180 Osm: 370 (Measured) Calcium 7.0 Toxicology Screen: Pending CXR: ET tube above carina, no infiltrates, no edema ECG: NSR, No ischemic changes
- 55.
- 56. Ethylene Glycol Poisoning Clinical Course: With a strong clinical suspicion for toxic alcohol ingestion, an ethanol drip is ordered, but due to pharmacy delay, the patient is orally loaded with whiskey obtained from another patient in the ER waiting room. Sodium Bicarbonate is administered for the profound acidosis and dialysis is initiated by the renal service . Ethylene glycol level of 310 mg/dl returns 12 hours later. The patient recovers with mild renal insufficiency, and is subsequently followed-up by the psychiatric service for his depression.
- 57. A 33-year-old manwith hemophilia and the AIDS had a six-hour history of severe right-sided flank pain and right-lower-quadrant pain accompanied by nausea, vomiting, and anorexia. The patient was afebrile and euvolemic. His medications included zidovudine, lamivudine, and indinavir. Urinalysis showed a specific gravity of 1.010, a pH of 5.0, and more than 50 red cells per high-power field.
- 58. A 33-year-old manwith hemophilia and the AIDS had a six-hour history of severe right-sided flank pain and right-lower-quadrant pain accompanied by nausea, vomiting, and anorexia. His medications included zidovudine, lamivudine, and indinavir. KUB x-ray following CT with IV contrast Urine under polarized microscopy
- 59. A CT scanwith IV contrast, obtained to assess the possibility of appendicitis and retroperitoneal bleeding, revealed a mildly dilated right renal collecting system. KUB x-ray following CT Polarized microscopy
- 60. To reduce therisk that the patient's strains of human immunodeficiency virus would become resistant if indinavir were withdrawn from the treatment regimen, the patient was instructed to continue taking the drug and to increase his fluid intake. Although his pain decreased initially, crystalluria persisted, and several weeks later, he returned with flank pain and hematuria. Ultrasonography at this time confirmed the development of several renal calculi. Treatment with indinavir was discontinued, and nelfinavir was added to his regimen of zidovudine and lamivudine. The renal calculi and crystalluria resolved spontaneously, and the patient was well at the time of the most recent follow-up visit.
- 61. Resumo Exame laboratorialmais antigo Permanece essencial: IRA IRC Infecção urinária Litíase DHEAB
Editor's Notes
- #3 Profetas da urina
- #4 No obstante, ninguna enseñanza médica del pasado fue tan importante ni tuvo uma influencia tan duradera como la de Claudio Galenus de Pérgamo, conocido simplemente como Galeno, quien en el siglo segundo DC unificó la medicina de su tiempo, dividida en una serie de grupos, en un sistema principal con su doctrina de la patología humoral: “No son los órganos sólidos el foco de las enfermedades sino los cuatro fluidos o humores corporales: sangre, cólera, flema y melancolía. Diabete – urinar no solo e aparecer formigas
- #11 In those clinical situations characterized by hypoxic tissues , there is an accumulation of reduced pyridine nucleotide and an increase asymmetrical presence of ketone in the form of beta- hydroxybutyrate . The importance of that point, obviously, is that the nitroprusside reaction in the tablet or in the dipstick will not respond to beta-hydroxybutyric acid but only responds to acetoacetic acid. Therefore, it is possible to have a diabetic in ketoacidosis, hypotensive, hypoxic, who has life- threatening degrees of ketoacidosis, but the ketones are being hidden in the form of the equally acidic beta-hydroxy butyrate. This hides it from the nitroprusside reaction, and you have a high anion gap acidosis in a diabetic. And as you increase tissue perfusion by expanding the intravascular volume, you now return the beta-hydroxybutyrate back to acetoacetate. The patient looks like he is getting better and the ketones are then all of a sudden getting very positive, simply reflecting the change in this steady state relationship between beta-hydroxy butyrate and acetoacetate.
- #16 Funcionais = exercício, ortostática
- #17 Biópsia líquida, obtida de forma indolor e não invasiva
- #18 Monomorphic hematuria (non-glomerular origin)
- #20 Phase contrast microscopy of glomerular bleeding. Acanthocytes are the ring forms with vesicle-shapped protrusions.
- #21 Scanning microscopy of glomerular bleeding. Acanthocytes are the ring forms with vesicle-shapped protrusions.
- #22 A kidney biopsy in a 34-year-old man with IgA nephropathy showed mesangial-cell proliferation and predominant mesangial IgA deposition. At the time of the biopsy, the patient's serum creatinine and blood urea nitrogen levels were 1.3 mg per deciliter (110 µmol per liter) and 13 mg per deciliter (4.6 mmol per liter), respectively. Microscopical examination of the urine revealed many dysmorphic urinary erythrocytes with spheroid surface protrusions (Panel A, x 1450) indicative of glomerular hematuria. A glomerular erythrocyte ghost (Panel B, x 3250) has a small neck at the base of each surface protrusion, demonstrating its connection with the cytoplasm of the cell. Urinary erythrocytes with surface protrusions such as those shown here are present in large numbers only with pathologic glomerular bleeding. (Differential interference contrast microscopy, x 1000).
- #26 This histologic section at medium power with trichrome stain highlights red blood cells grouping together in tubules to form casts. The tubular epithelium is also damaged, with a foamy appearance, and is the basis for the appearance of oval fat bodies in urine in this case.
- #28 Figure 1. Dysmorphic Red Cells in Urinary Sediment. Panel A shows red-cell casts (arrow) similar to the one seen in this patient. Panel B shows dysmorphic red cells (arrows), indicative of a glomerular lesion. (Photomicrographs from other patients, courtesy of Dirk Hentschel, Department of Nephrology, Massachusetts General Hospital.) Alport’s syndrome case from December 30 2004.
- #29 In Panel A (x 440), urinary sediment shows a red-cell cast and red cells. Red-cell casts indicate the presence of glomerular bleeding, a finding that is very specific but rather insensitive. If no red-cell casts are found, urinary red-cell morphology should be examined. The small, dysmorphic red cell (arrow) suggests a glomerular source, 15 and the uniform, biconcave disk shape of normal red cells (arrowhead) suggests nonglomerular bleeding. Some have noted that dysmorphic or abnormally shaped red cells are not reliable enough as a means for distinguishing a glomerular source of bleeding from a nonglomerular source, particularly if mixtures of dysmorphic and normal-appearing red cells are seen. 16,17 (Photomicrograph courtesy of the late Dr. Richard Nesson.) In Panel B (x 440), urinary sediment shows normal red cells (arrow) and crenated red-cell forms with spicules (arrowhead). Crenated red cells form in concentrated urine and are not diagnostically relevant. A more specific finding with bleeding of glomerular origin may be the presence of a particular form of abnormal red cells in the urine — acanthocytes, 18,19 doughnut-like cells with membrane blebs attached (Panel C, x 440, arrowhead). With meaningful acanthocyturia defined as the presence of acanthocytes accounting for more than 5 percent of urinary red cells, the sensitivity of phase microscopy for detecting glomerular hematuria was 52 percent in one large series in which glomerulonephritis was documented with renal biopsy and 73 percent in another series, and the specificity for detecting a glomerular source was 98 percent and 100 percent, respectively, in the two series. 18,19 The sensitivity and specificity of light microscopy for identifying acanthocytes have not been reported; since most laboratories do not routinely identify acanthocytes, this test should ideally be performed by an experienced laboratory technologist alerted to look for acanthocytes or by a nephrologist.
- #30 Figure 2. IgA Nephropathy. In Panel A, immunofluorescence microscopy reveals mesangial IgA in a 23-year-old man with recurrent hematuria ( x 320). In Panel B, light microscopy shows moderate expansion of the mesangial matrix with mild hypercellularity in the same patient (hematoxylin and eosin, x 156).
- #33 Sedimentoscopia na glomerulonefrite aguda
- #34 Figure 3. Poststreptococcal Glomerulonephritis. In Panel A, glomeruli from a 10-year-old girl with acute poststreptococcal glomerulonephritis show marked, diffuse hypercellularity, with infiltration of polymorphonuclear cells (hematoxylin and eosin, x 156). In Panel B, large, nodular, variegated subepithelial deposits referred to as &quot;humps&quot; (arrowheads) are present on electron microscopy ( x 9350).
- #35 Figure 4. Rapidly Progressive Glomerulonephritis. Panel A shows a glomerulus from a patient with rapidly progressive glomerulonephritis with a large crescent and compressed glomerular capillary tufts (hematoxylin and eosin, x 250). In Panel B, there is linear deposition of IgG along the glomerular basement membrane on immunofluorescence microscopy in a patient with circulating antibodies to glomerular basement membrane ( x 320).
- #39 Sedimentoscopia na pielonefrite aguda
- #41 Sedimentoscopia na síndrome nefrótica
- #42 Fatty casts can be distinguished from red cell casts because of the variability in size of the globules and maltese cross appearance under polarized light
- #43 Figure 3. Tubular-Cell Injury and Repair in Ischemic Acute Renal Failure. After ischemia and reperfusion, morphologic changes occur in the proximal tubules, including loss of the brush border, loss of polarity, and redistribution of integrins and Na/K–ATPase to the apical surface. Calcium, reactive oxygen species, purine depletion, and phospholipases probably have a role in these changes in morphology and polarity as well as in the subsequent cell death that occurs as a result of necrosis and apoptosis. There is a sloughing of viable and nonviable cells into the tubular lumen, resulting in the formation of casts and luminal obstruction and contributing to the reduction in the glomerular filtration rate. The severely damaged kidney can completely restore its structure and function. Spreading and dedifferentiation of viable cells occur during recovery from ischemic acute renal failure, which duplicates aspects of normal renal development. A variety of growth factors probably contribute to the restoration of a normal tubular epithelium.
- #44 Figure 1. Photomicrograph of Urinary Sediment Obtained from a Patient with Acute Tubular Necrosis ( x 200). Multiple broad, brown, granular casts are composed of Tamm–Horsfall glycoprotein, cells, remnants of shed brush border, and other cellular debris.
- #45 Casts which persist may break down, so that the cells forming it are degenerated into granular debris, as has occurred in this granular cast.
- #46 A 26-year-old man had sudden fever and chills with severe muscle pain and weakness in his legs and pectoral muscles while mountaineering in the Andes. He was brought to a local hospital, where he received hemodialysis three times because of anuria and a rapid rise in the serum creatinine level before being transferred to our unit. The following laboratory values were recorded on admission to our unit: creatinine, 10.5 mg per deciliter (928 µmol per liter); blood urea nitrogen, 85 mg per deciliter (30.3 mmol per liter); creatine kinase, 1990 U per liter; calcium, 8.16 mg per deciliter (2.04 mmol per liter); phosphorus, 6.19 mg per deciliter (2.0 mmol per liter); serum myoglobin, 283 µg per liter; and white-cell count, 14.5 x 10 3 per cubic millimeter. Urine dipstick analysis was positive (+++) for protein and red cells. Analysis of urinary sediment (Panel A; x 400) showed multiple pigmented casts, leukocyturia, and hematuria without dysmorphic red cells. Renal biopsy showed intratubular reddish-brownish, granular casts. Tubuli were slightly dilated, the tubular epithelium was flattened, and the glomeruli appeared normal. Intratubular casts were positive for myoglobin on immunoperoxidase staining (Panel B; x 400) with an antibody against human myoglobin, confirming the diagnosis of acute myoglobinuric renal failure. Possible causes of the rhabdomyolysis were physical strain at high altitude and the consumption of coca leaves and coca tea to prevent mountain sickness. No infectious cause could be identified. The patient had anuria or oliguria for 10 days. He received a total of seven sessions of hemodiafiltration, until urine flow returned and the serum creatinine levels began to fall. At the time of discharge, he had a serum creatinine level of 1.0 mg per deciliter (88.4 µmol per liter).
- #47 A 26-year-old man had sudden fever and chills with severe muscle pain and weakness in his legs and pectoral muscles while mountaineering in the Andes. He was brought to a local hospital, where he received hemodialysis three times because of anuria and a rapid rise in the serum creatinine level before being transferred to our unit. The following laboratory values were recorded on admission to our unit: creatinine, 10.5 mg per deciliter (928 µmol per liter); blood urea nitrogen, 85 mg per deciliter (30.3 mmol per liter); creatine kinase, 1990 U per liter; calcium, 8.16 mg per deciliter (2.04 mmol per liter); phosphorus, 6.19 mg per deciliter (2.0 mmol per liter); serum myoglobin, 283 µg per liter; and white-cell count, 14.5 x 10 3 per cubic millimeter. Urine dipstick analysis was positive (+++) for protein and red cells. Analysis of urinary sediment (Panel A; x 400) showed multiple pigmented casts, leukocyturia, and hematuria without dysmorphic red cells. Renal biopsy showed intratubular reddish-brownish, granular casts. Tubuli were slightly dilated, the tubular epithelium was flattened, and the glomeruli appeared normal. Intratubular casts were positive for myoglobin on immunoperoxidase staining (Panel B; x 400) with an antibody against human myoglobin, confirming the diagnosis of acute myoglobinuric renal failure. Possible causes of the rhabdomyolysis were physical strain at high altitude and the consumption of coca leaves and coca tea to prevent mountain sickness. No infectious cause could be identified. The patient had anuria or oliguria for 10 days. He received a total of seven sessions of hemodiafiltration, until urine flow returned and the serum creatinine levels began to fall. At the time of discharge, he had a serum creatinine level of 1.0 mg per deciliter (88.4 µmol per liter).
- #48 Analysis of urinary sediment (Panel A; x 400) showed multiple pigmented casts , leukocyturia, and hematuria without dysmorphic red cells. Renal biopsy showed intratubular reddish-brownish, granular casts . Tubuli were slightly dilated, the tubular epithelium was flattened, and the glomeruli appeared normal. Intratubular casts were positive for myoglobin on immunoperoxidase staining (Panel B; x 400) with an antibody against human myoglobin, confirming the diagnosis of acute myoglobinuric renal failure.
- #50 Sedimentoscopia na doença renal crônica
- #52 This is a broad, waxy cast. Note that the edges are sharp and there are &quot;cracks&quot; in this cast.
- #55 ETOH: 46
- #56 These are oxalate crystals, which look like little envelopes (or tetrahedrons, depending upon your point of view). Oxalate crystals are common. Struvite crystals (coffin lid). Normal urine is under-saturated with ammonium phosphate and struvite stone formation occurs only when ammonia production is increased and the urine pH is elevated to decrease the solubility of phosphate. Both of these requirements may be met when urinary tract infection occurs with a urease-producing organism, such as Proteus or Klebsiella.
- #57 Ethylene glycol itself is non toxic . It is metabolized to glycoaldehyde by alcohol dehydrogenase. Subsequent metabolites are glycolic acid and glyoxylic acid. The final metabolite is oxalate. Glycolic acid causes the metabolic acidosis. Oxalate precipitates with calcium.
- #58 A 33-year-old man with hemophilia and the acquired immunodeficiency syndrome had a six-hour history of severe right-sided flank pain and right-lower-quadrant pain accompanied by nausea, vomiting, and anorexia. The patient was afebrile and euvolemic. His medications included zidovudine, lamivudine, and indinavir. A computed tomographic scan with the intravenous administration of contrast medium, obtained to assess the possibility of appendicitis and retroperitoneal bleeding, revealed a mildly dilated right renal collecting system. This finding was confirmed by x-ray examination of the kidneys and upper bladder (Panel A), which provides a view equivalent to that of intravenous pyelography. Urinalysis showed a specific gravity of 1.010, a pH of 5.0, and more than 50 red cells per high-power field. Compensated polarizing microscopy showed indinavir crystal s in the urine (Panel B, x 100). To reduce the risk that the patient's strains of human immunodeficiency virus would become resistant if indinavir were withdrawn from the treatment regimen, the patient was instructed to continue taking the drug and to increase his fluid intake. Although his pain decreased initially, crystal luria persisted, and several weeks later, he returned with flank pain and hematuria. Ultrasonography at this time confirmed the development of several renal calculi. Treatment with indinavir was discontinued, and nelfinavir was added to his regimen of zidovudine and lamivudine. The renal calculi and crystal luria resolved spontaneously, and the patient was well at the time of the most recent follow-up visit.
- #59 A 33-year-old man with hemophilia and the acquired immunodeficiency syndrome had a six-hour history of severe right-sided flank pain and right-lower-quadrant pain accompanied by nausea, vomiting, and anorexia. The patient was afebrile and euvolemic. His medications included zidovudine, lamivudine, and indinavir. A computed tomographic scan with the intravenous administration of contrast medium, obtained to assess the possibility of appendicitis and retroperitoneal bleeding, revealed a mildly dilated right renal collecting system. This finding was confirmed by x-ray examination of the kidneys and upper bladder (Panel A), which provides a view equivalent to that of intravenous pyelography. Urinalysis showed a specific gravity of 1.010, a pH of 5.0, and more than 50 red cells per high-power field. Compensated polarizing microscopy showed indinavir crystal s in the urine (Panel B, x 100). To reduce the risk that the patient's strains of human immunodeficiency virus would become resistant if indinavir were withdrawn from the treatment regimen, the patient was instructed to continue taking the drug and to increase his fluid intake. Although his pain decreased initially, crystal luria persisted, and several weeks later, he returned with flank pain and hematuria. Ultrasonography at this time confirmed the development of several renal calculi. Treatment with indinavir was discontinued, and nelfinavir was added to his regimen of zidovudine and lamivudine. The renal calculi and crystal luria resolved spontaneously, and the patient was well at the time of the most recent follow-up visit.
- #60 A 33-year-old man with hemophilia and the acquired immunodeficiency syndrome had a six-hour history of severe right-sided flank pain and right-lower-quadrant pain accompanied by nausea, vomiting, and anorexia. The patient was afebrile and euvolemic. His medications included zidovudine, lamivudine, and indinavir. A computed tomographic scan with the intravenous administration of contrast medium, obtained to assess the possibility of appendicitis and retroperitoneal bleeding, revealed a mildly dilated right renal collecting system. This finding was confirmed by x-ray examination of the kidneys and upper bladder (Panel A), which provides a view equivalent to that of intravenous pyelography. Urinalysis showed a specific gravity of 1.010, a pH of 5.0, and more than 50 red cells per high-power field. Compensated polarizing microscopy showed indinavir crystal s in the urine (Panel B, x 100). To reduce the risk that the patient's strains of human immunodeficiency virus would become resistant if indinavir were withdrawn from the treatment regimen, the patient was instructed to continue taking the drug and to increase his fluid intake. Although his pain decreased initially, crystal luria persisted, and several weeks later, he returned with flank pain and hematuria. Ultrasonography at this time confirmed the development of several renal calculi. Treatment with indinavir was discontinued, and nelfinavir was added to his regimen of zidovudine and lamivudine. The renal calculi and crystal luria resolved spontaneously, and the patient was well at the time of the most recent follow-up visit.