Renal Disease Chapter 8 PDF

6/25/2024 RENAL DISEASE Chapter 8 PREAMBLE PowerPoints are a general overview and are provided to help students take notes over the video lecture ONLY. PowerPoints DO NOT cover the details needed for the Unit exam Each student is r...

6/25/2024 RENAL DISEASE Chapter 8 PREAMBLE PowerPoints are a general overview and are provided to help students take notes over the video lecture ONLY. PowerPoints DO NOT cover the details needed for the Unit exam Each student is responsible for READING the TEXTBOOK for details to answer the UNIT OBJECTIVES Unit Objectives are your study guide (not this PowerPoint) Test questions cover the details of UNIT OBJECTIVES found only in your Textbook! 1  6/25/2024 3 INTRODUCTION Disorders throughout the body can affect renal function and produce abnormalities in the urinalysis The kidneys are consistently exposed to potentially damaging substances Renal disease is classified as being glomerular, tubular, or interstitial GLOMERULAR DISORDERS 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, electrical charge interference, deposition of amyloid material and acute phase reactants, membrane thickening 2  6/25/2024 GLOMERULAR DISORDERS 5 (CONTINUED) 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 ACUTE POSTSTREPTOCOCAL 6 GLOMERULONEPHRITIS (AGN) Fever, edema around the eyes, fatigue, nausea, hypertension, oliguria, proteinuria, 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 Rapid anti–group A streptococcal enzyme tests Ease in diagnosis Decline in incidence 3  6/25/2024 RAPIDLY PROGRESSIVE (CRESCENTIC) 7 GLOMERULONEPHRITIS Systemic immune disorders Urinalysis similar to AGN May have increased fibrin Macrophages damage capillary progresses to more degradation products (FDP), More serious acute form → walls abnormal, elevated protein, cryoglobulins, and IgA renal failure Fibrin = permanent damage to low glomerular filtration immune complex capillary tufts rate (GFR) depositions 8 GOODPASTURE’S SYNDROME Morphological changes resembling crescentric GN Autoimmune disorder against glomerular and alveolar basement membranes Cytotoxic antibody following viral respiratory diseases Antiglomerular basement membrane antibody Hemoptysis, dyspnea, proteinuria, hematuria, RBC casts Chronic glomerulonephritis to end-stage renal failure is common 4  6/25/2024 GRANULOMATOSIS WITH POLYANGITIS Key to diagnosis Inflammation and Antineutrophilic cytoplasmic Formerly called Wegener granulomas in small blood antibody (ANCA) granulomatosis vessels of kidney and respiratory system Pulmonary symptoms first, Neutrophils initiate then hematuria, Immunofixation for p- immune response, proteinuria, RBC casts, ANCA/c-ANCA producing granulomas elevated BUN and creatinine levels HENOCH-SCHÖNLEIN PURPURA Children following upper respiratory infections Raised, red patches on skin Blood in sputum and 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 5  6/25/2024 MEMBRANOUS GLOMERULONEPHRITIS Systemic lupus IgG immune erythematosus complexes cause (SLE), Sjögren’s Slow progression, pronounced syndrome, Microscopic possible remission, thickening on secondary syphilis, hematuria, very nephrotic syndrome glomerular hepatitis B, gold and high protein frequently develops basement mercury treatments, membrane malignancy Often unknown etiology MEMBRANOPROLIFERATIVE 12 GLOMERULONEPHRITIS (MPGN) 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 Type 3: Subepithelial and subendothelial deposits Hematuria, proteinuria, ↓ serum complement Autoimmune disorders, infections, malignancies 6  6/25/2024 CHRONIC GLOMERULONEPHRITIS Progression from previous disorders Fatigue, anemia, hypertension, edema, oliguria gradually worsening Hematuria, proteinuria, glycosuria (tubular dysfunction), many types of casts including broad casts Markedly decreased GFR IMMUNOGLOBULIN A NEPHROPATHY (BERGER’S DISEASE) Most common cause of glomerulonephritis IgA complexes on glomerular membrane Increased serum levels of IgA Most frequently seen in children and young adults Early macroscopic hematuria from exercise or infection with spontaneous recovery Possibly asymptomatic for 20 years or more: gradual progression to chronic glomerulonephritis and ESRD 7  6/25/2024 15 NEPHROTIC SYNDROME Acute onset from systemic shock (low blood pressure) or glomerulonephritis complication Glomerular membrane damage and changes in podocyte electrical charges Protein passes through membrane; albumin depleted, causing increased lipid production Edema from loss of oncotic pressure Tubular and glomerular damage Possible progression of chronic renal failure URINALYSIS Marked proteinuria Fat droplets, oval fat bodies, renal epithelial cells, fatty and waxy casts, and casts, waxy casts, microscopic hematuria 8  6/25/2024 MINIMAL CHANGE DISEASE (LIPID NEPHROSIS OR NIL DISEASE) Children Heavy proteinuria, edema, transient hematuria; normal BUN and creatinine levels Most common cause of nephrotic syndrome-85%-95% Allergic reactions, immunization, HLA-B12 Good prognosis, steroids, remission FOCAL SEGMENTAL GLOMERULONEPHRITIS 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 and hepatitis 9  6/25/2024 ACUTE TUBULAR NECROSIS 19 Ischemia: severe decrease in blood flow Shock, trauma, surgery, surgical procedures Nephrotoxic agents: aminoglycosides, antibiotics, amphotericin B, cyclosporine, radiographic dye, ethylene glycol, heavy metals, toxic mushroom large amounts of hemoglobin and myoglobin Remove cause and manage symptoms Noticeable renal tubular epithelial (RTE) cells and casts and RTE fragments Hyaline, granular, waxy, broad casts 20 HEREDITARY AND METABOLIC TUBULAR DISORDERS Fanconi syndrome Generalized proximal convoluted tubule reabsorption failure Glucose, amino acids, phosphorus, sodium, potassium, bicarbonate and water most affected Inherited with cystinosis and Hartnup disease Acquired: heavy metals, outdated tetracycline Complication of multiple myeloma, renal transplant Glycosuria and mild proteinuria 10  6/25/2024 ALPORT’S SYNDROME 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, proteinuria, and renal insufficiency in later life to nephrotic syndrome and ESRD UROMODULIN ASSOCIATED KIDNEY 22 DISEASE (UMKD) Only protein produced by the kidney PCT and DCT 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 11  6/25/2024 DIABETIC NEPHROPATHY 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 glomerular matrix Deposition associated with glycosylated proteins from poorly controlled diet Sclerosis of vascular structure Reason for early microalbumin testing NEPHROGENIC DIABETES INSIPIDUS Nephrogenic: failure of tubules to respond to antidiuretic hormone Two types (ADH) Neurogenic: failure to produce ADH Nephrogenic DI-Inherited sex- linked recessive gene, medications (lithium and amphotericin B) Urine: low specific gravity (SG), pale yellow color, possible false- negative results for other tests 12  6/25/2024 RENAL GLYCOSURIA 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 26 URINARY TRACT INFECTION Most common renal disease is urinary Cystitis (bladder infection) is very tract infection (UTI) common Untreated: progresses to more serious upper urinary tract Commonly seem in women and children Urinary frequency and burning Many WBCs, bacteria, increased pH, mild proteinuria, hematuria 13  6/25/2024 ACUTE 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 CHRONIC PYELONEPHRITIS 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, ↓ renal concentration 14  6/25/2024 ACUTE INTERSTITIAL NEPHRITIS Allergic reaction causing inflammation of interstitium Medication allergy to penicillin, methicillin, ampicillin, cephalosporins, rifampin, sulfonamides, NSAIDs, thiazide diuretics Discontinue and use steroids to treat Urinalysis, hematuria, proteinuria,↑ WBCs, WBC casts, no bacteria Staining for eosinophils RENAL FAILURE Acute and chronic forms Chronic renal failure Progression from original disorders to end-stage renal disease GFR