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Copyright © 2014. F.A. Davis Company
CHAPTER 7CHAPTER 7
RENAL DISEASERENAL DISEASE
Copyright © 2014. F.A. Davis Company
Upon completing this chapter, the reader will be able to1.Differentiate among renal diseases of glomerular, tubular, interstitial, and vascular origin.2.Describe the processes by which immunologic damage is caused to the glomerular basement membrane.3.Define glomerulonephritis.4.Describe the characteristic clinical symptoms, etiology, and urinalysis findings in acute poststreptococcal and rapidly progressive glomerulonephritis, Goodpasture syndrome, Wegener’s granulomatosis, and Henoch-Schönlein purpura. 5.Name three renal disorders that also involve acute respiratory symptoms.
Learning ObjectivesLearning Objectives
Copyright © 2014. F.A. Davis Company
6. Differentiate between membranous and membranoproliferative glomerulonephritis.
7. Discuss the clinical course and significant laboratory results associated with immunoglobulin A nephropathy.
8. Relate laboratory results associated with the nephrotic syndrome to the disease process.
9. Compare and contrast the nephrotic syndrome and minimal change disease with regard to laboratory results and course of disease.
10. State two causes of acute tubular necrosis.11. Name the urinary sediment constituent most diagnostic of renal
tubular damage.
Learning Objectives Learning Objectives (cont’d)(cont’d)
Copyright © 2014. F.A. Davis Company
12. Describe Fanconi syndrome, Alport syndrome, uromodulin-associated renal disease, and renal glucosuria.
13. Differentiate between diabetic nephropathy and nephrogenic diabetes insipidus.
14. Compare and contrast the urinalysis results in patients with cystitis, pyelonephritis, and acute interstitial nephritis.
15. Differentiate among causes of laboratory results associated with prerenal, renal, and postrenal acute renal failure.
16. Discuss the formation of renal calculi, composition of renal calculi, and patient management techniques.
Learning Objectives Learning Objectives (cont’d)(cont’d)
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• Disorders throughout the body can affect renal function and produce abnormalities in the urinalysis
• The kidneys are consistently exposed to potentially damaging substances
IntroductionIntroduction
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• Glomerular disorders• Tubular disorders• Interstitial disorders
ClassificationClassification
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• Majority are of immunologic disorders– Immune complexes from immunologic reactions
throughout the body– Increased serum immunoglobulins are deposited on the
glomerular membranes– Immune system mediators: complement migrate and
produce change and damage to membranes• Nonimmunologic
– Chemicals and toxins, deposition of amyloid material and acute phase reactants, electrical charge interference, membrane thickening
Glomerular DisordersGlomerular Disorders
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Glomerular Disorders Glomerular Disorders (cont’d)(cont’d)
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• Glomerulonephritis– General term for sterile, inflammatory process
affecting the glomerulus– Causes blood, protein, and casts in urine
• Types of glomerulonephritis progress through various disorders– Acute glomerulonephritis to chronic
glomerulonephritis to nephrotic syndrome to renal failure
Glomerular Disorders Glomerular Disorders (cont’d)(cont’d)
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• Fever, edema around the eyes, oliguria, and hematuria• Immune complexes deposit on glomerular membranes• Hematuria, proteinuria, oliguria
– Red blood cell (RBC) casts, dysmorphic RBCs– Hyaline and granular casts– White blood cells – Anti–group A streptococcal enzyme tests
• Group A streptococcal infections from organisms with M protein in the cell wall
• Rapid anti–group A streptococcal enzyme tests– Ease in diagnosis– Decline in incidence
Acute Poststreptococal Acute Poststreptococal Glomerulonephritis (AGN)Glomerulonephritis (AGN)
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• More serious acute form → renal failure• Systemic immune disorders
– Macrophages damage capillary walls– Fibrin = permanent damage to capillary tufts
• Urinalysis similar to AGN progresses to more abnormal, elevated protein, low glomerular filtration rate (GFR)
• May have increased fibrin degradation products (FDP), cryoglobulins and IgA immune complex depositions
Rapidly Progressive (Crescentic) Rapidly Progressive (Crescentic) GlomerulonephritisGlomerulonephritis
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• Morphological changes resembling crescentric GN• Autoimmune disorder against glomerular and
alveolar basement membranes• Cytotoxic antibody following viral respiratory
diseases– Antiglomerular basement membrane antibody
• Hemoptysis, hematuria, proteinuria, RBC casts• Chronic glomerulonephritis to end-stage renal
failure is common
Goodpasture’s SyndromeGoodpasture’s Syndrome
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• Inflammation and granulomas in small blood vessels of kidney and respiratory system
• Key to diagnosis– Antineutrophilic cytoplasmic antibody (ANCA)
• Neutrophils initiate immune response, producing granulomas
• Pulmonary symptoms first, then hematuria, proteinuria, RBC casts, elevated BUN and creatinine levels
• Immunofixation for p-ANCA/c-ANCA
Wegener’s GranulomatosisWegener’s Granulomatosis
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• Children following upper respiratory infections• Raised, red patches on skin• Blood in sputum and possibly stools • Renal involvement is the most serious complication
of the disorder– Proteinuria and hematuria, RBC casts
• 50% complete recovery• Follow patients for more serious renal problems
Henoch-Schönlein PurpuraHenoch-Schönlein Purpura
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• IgG immune complexes cause pronounced thickening on glomerular basement membrane
• Systemic lupus erythematosus, Sjögren’s syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy– These aid in diagnosis– Often unknown etiology
• Slow progression, remission, nephrotic syndrome• Microscopic hematuria, very high protein
Membranous GlomerulonephritisMembranous Glomerulonephritis
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• Type 1: increased cellularity in the subendothelial cells of the mesangium– Thickening of capillary walls
• Type 2: extremely dense deposits in the glomerular basement membrane– Poor prognosis
• Hematuria, proteinuria, ↓ complement• Autoimmune disorders, infections, malignancies
Membranoproliferative Membranoproliferative Glomerulonephritis (MPGN)Glomerulonephritis (MPGN)
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Chronic GlomerulonephritisChronic Glomerulonephritis
• Progression from previous disorders
• Fatigue, anemia, hypertension, edema, oliguria gradually worsening
• Hematuria, proteinuria, glycosuria (tubular damage), many types of casts including broad and waxy casts
• Markedly decreased GFR
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• Most common cause of glomerulonephritis• IgA complexes on glomerular membrane• Increase serum IgA• Early macroscopic hematuria from exercise or
infection with spontaneous recovery• 20 years later: gradual progression to chronic
glomerulonephritis• Granular and disintegrating RBC casts
Immunoglobulin A Nephropathy Immunoglobulin A Nephropathy (Berger’s Disease)(Berger’s Disease)
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• Acute onset from systemic shock (low blood pressure) or glomerulonephritis complication
• Glomerular membrane damage and changes in podocyte electrical charges
• Protein passes through membrane; serum albumin depleted, causing increased lipid production
• Edema from loss of oncotic pressure• Tubular damage
Nephrotic SyndromeNephrotic Syndrome
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UrinalysisUrinalysis
• Marked proteinuria >3.5 g/day
• Fat droplets, oval fat bodies, fatty casts, renal tubular epithelial cells and casts, waxy casts, microscopic hematuria
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• Children, allergic reactions, immunization, HLA-B12
• Heavy proteinuria, edema, transient hematuria; normal BUN and creatinine levels
• Good prognosis, steroids, remission
Minimal Change Disease Minimal Change Disease (Lipid Nephrosis)(Lipid Nephrosis)
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• Similar to nephrotic syndrome but affects only certain numbers and areas of glomeruli; podocytes are damaged
• IgM and C3 immune deposits• Moderate to heavy proteinuria; microscopic
hematuria• Heroin and analgesic abuse, HIV
Focal Segmental Focal Segmental Glomerulonephritis Glomerulonephritis
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• Inherited sex-linked and autosomal disorder affecting basement membrane
• Males more severely affected• Macroscopic hematuria with respiratory infections
by age 6 years• Membrane laminated with thinning; no immune
complexes• Mild to persistent hematuria, later nephrotic
syndrome, renal failure for some
Alport’s SyndromeAlport’s Syndrome
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• Formerly Tamm-Horsfal protein is the only protein produced by the kidney
• Inherited disorder that results in an abnormal buildup of uromodulin in the tubular cells causing their destruction
• Patients have elevated serum uric acid and gout at an early age, occurs before renal symptoms
Uromodulin Associated Kidney Uromodulin Associated Kidney Diseases (UMKD)Diseases (UMKD)
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• Most common cause of end-stage renal disease• Glomerular basement membrane thickening• Increased proliferation of mesangial cells• Increased deposition of cellular and acellular material within
matrix of Bowman’s capsule and around capillary tufts• Deposition associated with glycosylated proteins from poorly
controlled diet• Sclerosis of vascular structure• Reason for early microalbumin testing
Diabetic NephropathyDiabetic Nephropathy
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Acute Tubular NecrosisAcute Tubular Necrosis
• Ischemia: severe decrease in blood flow
– Trauma, surgery, cardiac failure, electricity, toxogenic bacteria, anaphylaxis
• Nephrotoxic agents: aminoglycosides, amphotericin B, ethylene glycol, heavy metals, mushroom poisoning, hemoglobin, myoglobin
• Remove cause and manage symptoms• Noticeable renal tubular epithelial
(RTE) cells and casts and RTE fragments
• Hyaline, waxy, granular, broad casts
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• Fanconi syndrome– Generalized proximal convoluted tubule reabsorption
failure– Inherited with cystinosis and Hartnup disease– Acquired: heavy metals, outdated tetracycline– Complication of multiple myeloma, renal transplant– Glycosuria and electrolyte imbalance
Hereditary and Metabolic DisordersHereditary and Metabolic Disorders
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• Two types1. Nephrogenic: failure of tubules to respond to
antidiuretic hormone (ADH), inherited sex-linked recessive or lithium and amphotericin B exposure, polycystic kidneys and sickle cell anemia
2. Neurogenic: failure to produce ADH
• Urine: pale yellow, low specific gravity (SG), possible negative results for other tests
Nephrogenic Diabetes InsipidusNephrogenic Diabetes Insipidus
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• Affects only the reabsorption of glucose• Inherited as autosomal recessive• Decreased number of glucose transporters in
tubules• Decreased affinity of transporters for glucose• Glycosuria with normal blood glucose level
Renal GlycosuriaRenal Glycosuria
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• Infections and inflammations affecting the interstitium and the tubules
• Most common renal disease is urinary tract infection (UTI)
• Cystitis (bladder infection) is very common– Untreated: progresses to upper urinary tract– Many WBCs, bacteria, increased pH, mild proteinuria,
hematuria– WBCs in urine called pyuria
Tubulointerstitial DiseasesTubulointerstitial Diseases
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Acute PyelonephritisAcute Pyelonephritis
• Ascending movement of bacteria– Conditions affecting emptying
of bladder– Calculi, pregnancy, reflux of
urine from bladder to ureters• Rapid onset, urinary
frequency, burning, lower back pain
• Urinalysis: similar to cystitis with one exception: presence of WBC casts
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• Damage to tubules, possible renal failure• Congenital structural defects causing reflux are
most common cause• Can affect emptying of collecting ducts• Often diagnosed in children• Early urinalysis similar to acute pyelonephritis• Later granular, waxy, and broad casts; increased
protein, hematuria, ↓ SG
Chronic PyelonephritisChronic Pyelonephritis
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Acute Interstitial NephritisAcute Interstitial Nephritis• Allergic reaction causing
inflammation of interstitium and tubules
• Medication allergy to penicillin, methicillin, ampicillin, cephalosporins, NSAIDs, thiazide diuretics
• Discontinue and use steroids to treat
• Urinalysis, hematuria, proteinuria,↑ WBCs, WBC casts, no bacteria
• Hansel stain for eosinophils
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• Acute and chronic forms• Chronic renal failure
– Progression from original disorders to end-stage renal disease
– GFR <25 mL/min, ↑↑ BUN and creatinine levels, electrolyte imbalance, isosthenuria, proteinuria, renal gycosuria; ↑ granular, waxy, broad casts
Renal FailureRenal Failure
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• Sudden onset, often reversible• Decreased blood flow (prerenal), acute disease
(renal), renal calculi and tumors (postrenal)• Urinalysis related to cause
– RTE cells = decreased blood flow– RBCs = glomerular damage– WBCs and casts = infection/inflammation– Urothelial cells = possible bladder tumor
Acute Renal FailureAcute Renal Failure
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• Prerenal– Decreased blood pressure/cardiac output– Hemorrhage– Burns– Surgery– Septicemia
• Renal– Acute glomerulonephritis– Acute tubular necrosis– Acute pyelonephritis– Acute interstitial nephritis
Causes of Acute Renal FailureCauses of Acute Renal Failure
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• Postrenal– Renal calculi– Tumors– Crystallization of ingested substances
Causes of Acute Renal Failure Causes of Acute Renal Failure (cont’d)(cont’d)
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• Renal calculi (kidney stones) in calyces and pelvis of kidney, ureters, bladder
• Staghorn, round and smooth, barely seen• Severe back pain radiating from lower back to
legs when passing• Lithotripsy: high-energy shock waves break up
stones• Also surgical removal
Renal LithiasisRenal Lithiasis
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• Formation conditions similar to crystals– pH, concentration, urine stasis– No exact cause of formation known– Increased in the summer, dehydration
• Types of stones– 75% calcium oxalate or phosphate– Magnesium ammonium phosphate (stuvite)
• UTI and ↑ pH, like triple phosphate crystals– Uric acid: increased purine diet– Cystine: hereditary cystinosis
Renal Lithiasis Renal Lithiasis (cont’d)(cont’d)