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Urology/Nephrology

Urology/Nephrology. Lecture Four – February 28, 2013. Renal Cell Carcinoma. Renal Cell Carcinoma. 2.6% of all adult cancers 52,190 diagnoses and 12,890 deaths each year Peaks in 6 th decade of life; male-to-female 2:1 Only significant environmental risk factor – smoking

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Urology/Nephrology

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  1. Urology/Nephrology Lecture Four – February 28, 2013

  2. Renal Cell Carcinoma

  3. Renal Cell Carcinoma • 2.6% of all adult cancers • 52,190 diagnoses and 12,890 deaths each year • Peaks in 6th decade of life; male-to-female 2:1 • Only significant environmental risk factor – smoking • Familial predisposition, dialysis-related cystic disease, genetic abberation can all contribute • Sporadic tumors are most common • Originate from proximal tubule cells

  4. Renal Cell Carcinoma • Signs and Symptoms – 60% with gross or microscopic hematuria; 30% with flank pain or abdominal mass • Triad of flank pain, hematuria, mass – 10-15% - advanced • Fever—paraneoplastic symptom • Metastatsis (cough, bone pain) – 30% • Increased diagnosis incidentally due to increased use of abdominal imaging • Labs—hematuria (60%), erythrocytosis in 5% (anemia is more common); hypercalcemia; Stauffer syndrome • Imaging – abdominal US or CT (most valuable), CXR, bone scans, doppler US

  5. Renal Cell Carcinoma • Radical nephrectomy – primary treatment for localized RCC • Partial nephrectomy – single kidney, renal disease, or bilateral cancerous lesions • No effective chemotherapy for metastatic RCC • Prognosis varies with spread of disease • T1-T2 (confined to renal capsule) – 90-100% survival at 5 yrs • T3-T4 50-60% survival • Node-positive tumors – 0-15% survival • Solitary localized metastasis – 15-30% survival Note – Read Angiomyolipomas p. 1594

  6. Polycystic Kidney Disease

  7. Polycystic Kidney Disease • One of the most common hereditary diseases (1 in 800) • 50% of pts have ESRD by age 60 • 10% of dialysis patients in the US • 85-90% of pts have mutation in ADPKD1 on short arm of chromosome 16 • 10-15% of pts have mutation in ADPKD 2 on chromosome 4 – slower disease progression and longer life expectancy

  8. Polycystic Kidney Disease • Abdominal or flank pain • Microscopic or gross hematuria • History of UTIs and/or nephrolithiasis • Family history of PCKD in 75% • 50% or more may have HTN • May have large, palpable kidneys on exam • 40-50% -- concurrent hepatic cysts; may also see pancreatic or splenic cysts • H&H usually normal • Urinalysis – hematuria, proteinuria

  9. Polycystic Kidney Disease • US confirms diagnosis • 2+ cysts in pts <30 (88.5% sensitive) • 2+ cysts in each kidney in pts 30-59 (100% sensitive) • 4+ cysts in each kidney in pts 60 or older • If US results unclear, CT is highly sensitive

  10. Polycystic Kidney Disease • Pain – abdomen or flank; from bleeding into cysts, infection and nephrolithiasis • bed rest or analgesia; cyst decompression • Hematuria – rupture of cyst, kidney stone, UTI; resolves in 7 days with bed rest and hydration • Recurrent – possible RCC – especially in men >50 y/o • Infection – flank pain, fever, leukocytosis, +/- blood cultures, +/- normal UA; CT scan may help diagnose • Antibiotics with good cystic penetration – Bactrim, fluoroquinolones – may need 2 weeks of IV therapy and long-term oral therapy • Nephrolithiasis – in up to 20% of pts • 2-3 L/day hydration

  11. Polycystic Kidney Disease • Hypertension – 50% at presentation, most will eventually developduring disease • Cyst-induced ischemia – RAAS activation • Cyst decompression can improve, plus oral medication • Cerebral Aneurysms – 10-15% have aneurysms on Circle of Willis; screening arteriography not recommended unless + family history • Mitral valve prolapse (up to 25%), aortic aneurysms, aortic valve disease, colonic diverticula • Research continues regarding therapy • Avoiding caffeine, treating HTN, low-protein diet may help

  12. Glomerulonephritis

  13. Nephritic Spectrum Glomerular Diseases • Glomerulonephritis—inflammatory process  renal dysfunction • Acute (days—weeks), with or without resolution • Chronic with progressive scarring • See Figure 22-4 p. 894 • Symptoms/signs • If nephritic syndrome present, edema is first seen in low tissue pressure regions (periorbital and scrotal areas) • HTN—sodium retention from acute decrease in GFR • Heavy glomerular bleedinggross hematuria (smoky or cola urine)

  14. Nephritic Spectrum Glomerular Disorders

  15. Nephritic Spectrum Glomerular Disorders • Labs—may do complement, ANA, cryoglobulins, hepatitis panel, ANCA, anti-GBM antibodies, ASO titers based on H&P • Urinalysis—protein, dysmorphic RBCs (abnormal from crossing damaged capillary membrane); RBC casts; proteinura usually <3 grams/day • Biopsy—consider if no contradindications • Treatment—aggressive treatment of hypertension and fluid overload; may need dialysis

  16. Postinfectious Glomerulonephritis • Usually due to infectious with nephritogenic GABHS • Commonly 1-3 wks after pharyngitis or impetigo • Other causes—bacteremia, bacterial pneumonia, deep-seated abscess, Gram-negative infections, infective endocarditis, and shunt infections • Viral, fungal, and parasitic infections can also cause

  17. Postinfectious Glomerulonephritis • Signs/Symptoms—varies widely from asymptomatic glomerular hematuria to nephritic syndrome • Labs—Low serum complement, may see elevated antistreptolysin-O titers; glomerular hematuria; subnephrotic proteinuria; elevated serum creatinine; red cell casts in urine • renal biopsy shows diffuse proliferative pattern of injury • immunofluorescence shows IgG and C3 in granular pattern in mesangium and along capillary basement membrane • Electron microscopy shows large, dense subepithelial deposits

  18. Postinfectious Glomerulonephritis

  19. Postinfectious Glomerulonephritis • Treatment—Underlying infection should be identified and treated appropriately • Supportive tx—anti-hypertensives, salt restrictions, diuretics • Corticosteroids do not improve outcome • Prognosis depends on severity of injury and age of patient • Children—more likely to fully recover • Adults—prone to development of severe disease and CKD

  20. IgA Nephropathy • Berger disease • Primary renal diseaseIgA deposits in glomerular mesangium • Associated with hepatic cirrhosis, celiac disease, HIV, CMV • Most common primary glomerular disease worldwide • most common in children and young adults • males 2-3 times more commonly affected than women

  21. IgA Nephropathy • Signs and Symptoms—episode of gross hematuria is the most common presenting symptom • May see with URI (50%), GI symptoms (10%), flu-like illness (15%) • Red or cola-colored urine 1-2 days after onset • Can range from asymptomatic microscopic hematuria to rapidly progressive glomerulonephritis • No serologic tests can help diagnose • Treatment—if >1g/d proteinuria, ACE or ARB • Target BP <130/80 mmHg, target proteinuria <500 mg/d • If 1-3.5 g/d proteinuria and GFR >70 mL/min, steroids may be helpful • Others—fish oil, kidney transplant if ESRD • Prognosis—1/3 with spontaneous remission, progressive CKD in 40-50%, remainder with chronic microscopic hematuria and stable Cr

  22. Other forms of glomerulonephritis • Henloch-SchönleinPurpura—small vessel leukocytoclasticvasculitis; IgA in vessel walls • most commonly in children after an infection • Palpable purpura of LE and buttocks, arthralgia, abdominal symptoms • Pauci-immune glomerulonephritis—(ANCA associated)—Wegener granulomatosis, Churg-Strauss disease, and microscopic polyangiitis • Signs and symptoms of systemic inflammatory disease • Antiglomerular Basement Membrane Glomerulonephritis and Goodpasture Syndrome • Antibodies to epitopes in the glomerular basement membrane

  23. Nephrotic Syndrome

  24. Nephrotic Syndrome • 1/3 of patients with nephrotic syndrome have systemic disease • DM, amylodosis, SLE • Remainder—primary renal disease • Signs and Symptoms—peripheral edema is hallmark • Occurs when serum albumin is <3 g/L • When serum albumin <2 g/dL, arterial underfilling from low plasma oncotic pressure • Initially in dependent areas, but can become generalized, including periorbital edema • Dyspnea  pulmonary edema, pleural effusion, diaphragmatic compromise due to ascites • Increased infections  loss of Ig and complement • Increased thrombotic events  loss of anticoagulant factors

  25. Nephrotic Syndrome

  26. Nephrotic Syndrome—Labs • Urinalysis—proteinuria • Spot urine protein to urine creatine ratio—approximate grams/day of protine lost in urine • few casts or cells—may have oval fat bodies from lipid deposits in sloughed renal tubular epithelial cells • “grape clusters” or “Maltese crosses”

  27. Nephrotic Syndrome—Labs • Blood Chemistries—hypoalbuminemia (<3 g/dL) and hypoproteinemia (<6 d/dL) • Hyperlipidemia50% of patients with early nephrotic syndrome and more common as disease becomes more severe • Elevated erythrocyte sedimentation rate • Deficiency in vitamin D, zinc, and copper loss • Renal biopsy—to identify underyling cause—table 22-10 • Mainly to see if there is a primary renal disease that may require or respodne to drug therapy • Chronically and significantly elevated creatinine levels—irreversible kidney disease—biopsy likely not helpful • Biopsy rarely done in setting of longstanding DM

  28. Nephrotic Syndrome—Treatment • Protein Loss—dietary protein intake should replace daily urinary protein losses • Protein malnutrition mainly with urinary protein losses >10 g/day • May be mild renal benefit to protein restriction—recommend 0.6-0.8 g/kg/day if GFR <25 mL/min • ACE and ARB reduce protein excretion—can use with caution in patients with reduced GFR • Edema—dietary salt restriction, diuretics (thiazides, loops) • Hyperlipidemia—dietary modification, exercise, medication • Statins are cleared by liver, but pts with CKD are more prone to rhabdomyolysis if taking gemfibrozil plus a statin • Hypercoagulable state—serum albumin <2 g/dL • Anticoagulants for 3-6 months in patients with evidence of thrombosis in any location

  29. Questions?

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