copyright © 2014. f.a. davis company chapter 7 renal disease

Copyright © 2014. F.A. Davis Company

CHAPTER 7CHAPTER 7

RENAL DISEASERENAL DISEASE


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


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)


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)


• Disorders throughout the body can affect renal function and produce abnormalities in the urinalysis

• The kidneys are consistently exposed to potentially damaging substances

IntroductionIntroduction


• Glomerular disorders• Tubular disorders• Interstitial disorders

ClassificationClassification


• 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


Glomerular Disorders Glomerular Disorders (cont’d)(cont’d)


• 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)


• 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)


• 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


• 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


• 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


• 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


• 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


• 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)


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


• 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)


• 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


UrinalysisUrinalysis

• Marked proteinuria >3.5 g/day

• Fat droplets, oval fat bodies, fatty casts, renal tubular epithelial cells and casts, waxy casts, microscopic hematuria


• 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)


• 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


• 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


• 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)


• 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


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


• 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


• 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


• 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


• 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


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


• 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


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


• 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


• 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


• 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


• Postrenal– Renal calculi– Tumors– Crystallization of ingested substances

Causes of Acute Renal Failure Causes of Acute Renal Failure (cont’d)(cont’d)


• 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


• 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)

copyright © 2014. f.a. davis company chapter 7 renal disease

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