Renal Diseases Lecture Notes PDF

RENAL DISEASES MT104 - AUBF LAWRENCE R. SANTIAGO, RMT Introduction  Disorders throughout the body can affect renal function and produce abnormalities in the urinalysis. Considering that the major function of the kidneys is filtration of the blood to remove waste products, it becomes evident t...

RENAL DISEASES MT104 - AUBF LAWRENCE R. SANTIAGO, RMT Introduction  Disorders throughout the body can affect renal function and produce abnormalities in the urinalysis. Considering that the major function of the kidneys is filtration of the blood to remove waste products, it becomes evident that the kidneys are consistently exposed to substances that are potentially damaging.  Oftenrenal disease is classified as being glomerular, tubular, or interstitial, based on the area of the kidney primarily affected. Glomerular Disorders  result from immunologic disorders  formed immune complexes as a result of immunologic reactions and increased serum immunoglobulins (IgA) - deposited in the glomerular membranes  complement, neutrophils, lymphocytes, monocytes, and cytokines are attracted to the deposit area damaging the membranes  damage may consist of cellular infiltration or proliferation, resulting in thickening of the glomerular basement membrane, as well as complement-mediated damage to the capillaries and basement membrane Continued Nonimmunologic causes of glomerular damage include the following: Exposure to chemicals and toxins that also affect the tubules Disruption of the electrical membrane charges as occurs in nephrotic syndrome (NS) Deposition of amyloid material from systemic disorders that may involve chronic inflammation and acute-phasereactants Thickening of the basement membrane associated with diabetic nephropathy Glomerulonephritis  Sterile, inflammatory process the glomerulus.  Associated with the finding of blood, protein, and casts in the urine A variety of types of glomerulonephritis exist, and the condition also may progress from one form to another (i.e., rapidly progressive glomerular nephritis, to chronic glomerulonephritis, to nephrotic syndrome and eventual renal failure) Acute Poststreptococcal Glomerulonephritis  Acute glomerulonephritis (AGN)  Marked by the sudden onset of symptoms consistent with damage to the glomerular membrane. (fever, edema most noticeably around the eyes, fatigue, nausea, hypertension, oliguria, proteinuria, and hematuria)  Symptoms usually occur in children and young adults after respiratory infections caused by certain strains of group A β-hemolytic streptococci that contain M protein in the cell wall. continued  nephrogenic strains of streptococci form immune complexes with their corresponding circulating antibodies and become deposited on the glomerular membranes. The accompanying inflammatory reaction affects glomerular function.  treatment involves successful management of the secondary complications (hypertension and electrolyte imbalance) until the immune complexes have been cleared from the blood and the inflammation subsides, resulting in no permanent damage to the kidney. Acute glomerulonephritis - urinalysis findings  marked hematuria, proteinuria, and oliguria, accompanied by red blood cell (RBC) casts, dysmorphic RBCs, hyaline and granular casts, and white blood cells (WBCs).  Blood urea nitrogen (BUN) may be elevated during the acute stages  positive for Antistreptolysin O (ASO) - anti group-A strep enzyme test  As toxicity to the glomerular membrane subsides, urinalysis results return to normal, with the possible exception of microscopic hematuria that lasts until the membrane damage has been repaired.  RBC casts are a hallmark characteristic of acute glomerulonephritis. Rapidly Progressive (Crescentic) Glomerulonephritis  a much poorer prognosis, often terminating in renal failure  Symptoms are initiated by deposition of immune complexes in the glomerulus, often as a complication of another form of glomerulonephritis or a disorder of the immune system, such as systemic lupus erythematosus (SLE)  Damage by macrophages to the capillary walls releases cells and plasma into Bowman space, and the production of crescentic formations containing macrophages, fibroblasts, and polymerized fibrin causes permanent damage to the capillary tufts. Rapidly Progressive (Crescentic) Glomerulonephritis - urinalysis findings  laboratory results are similar to AGN but become more abnormal as the disease progresses  protein levels that are markedly elevated  glomerular filtration rates that are very low Goodpasture Syndrome  Morphological changes to the glomeruli resembling those in rapidly progressive glomerular nephritis are seen in conjunction with the autoimmune disorder termed Goodpasture syndrome  A cytotoxic autoantibody can appear against the glomerular and alveolar basement membranes after viral respiratory infections.  Attachment of this autoantibody to the basement membrane, followed by complement activation, produces the capillary destruction  antiglomerular basement membrane antibody, the autoantibody can be detected in patient serum  Initial pulmonary complaints are hemoptysis and dyspnea, followed by the development of hematuria. Goodpasture Syndrome - Urinalysis findings  proteinuria  hematuria  presence of RBC casts.  Progressionto chronic glomerulonephritis and end-stage renal failure is common. Granulomatosis With Polyangiitis (GPA)  Formerly called Wegener granulomatosis  Granuloma-producing inflammation of the small blood vessels, primarily of the kidney and respiratory system.  Antineutrophilic cytoplasmic antibody (ANCA) in the patient’s serum leads to diagnosis  Pulmonary symptoms present first and later develop renal involvement, including hematuria, proteinuria, RBC casts, and elevated levels of serum creatinine and BUN Continued  Testing for ANCA: serum incubation with ethanol or formalin/formaldehyde fixed neutrophils  Examining the preparation using indirect immunofixation to detect the serum antibodies attached to the neutrophils.  If the neutrophils are fixed in ethanol, the antibodies form a perinuclear pattern called p-ANCA. When the neutrophils are fixed with formalin/formaldehyde, the pattern is granular throughout the cytoplasm and is referred to as c-ANCA. Henoch-Schönlein Purpura  occurs primarily in children after upper respiratory infections  symptoms include the appearance of raised, red patches on the skin.  Respiratory and gastrointestinal symptoms, including blood in the sputum and stools, may be present  Renal involvement is the most serious complication of the disorder and may range from mild to heavy proteinuria and hematuria with RBC casts. Membranous Glomerulonephritis A pronounced thickening of the glomerular basement membrane resulting from the deposition of immunoglobulin G immune complexes  Disorders associated with membranous glomerulonephritis development include SLE, Sjögren syndrome, secondary syphilis, hepatitis B  Laboratory findings: microscopic hematuria, elevated protein excretion, rare RBC casts. Membranoproliferative Glomerulonephritis  marked by different alterations in the cellularity of the glomerulus and peripheral capillaries  Type 1 displays increased cellularity in the subendothelial cells of the mesangium (interstitial area of Bowman capsule), causing thickening of the capillary walls.  Type 2 (dense deposit disease) displays extremely dense deposits in the glomerular basement membrane, tubules, and Bowman capsule  Type 3 is characterized by both subepithelial and subendothelial deposits. Continued  Patients are mostly children  Poor prognosis  Type 1 patients progress to nephrotic syndrome  Type 2 patients experience symptoms of chronic glomerulonephritis after renal transplant Membranoproliferative Glomerulonephritis - Lab findings  hematuria  proteinuria  decreased serum complement levels  association with autoimmune disorders, infections, and malignancies Chronic Glomerulonephritis  Damage to the glomerulus may progress to chronic glomerulonephritis (CGN) and end- stage renal disease (ESRD)  Gradually worsening symptoms include fatigue, anemia, hypertension, edema, and oliguria Chronic Glomerulonephritis - lab findings  hematuria  proteinuria  glucosuria  presence of broad casts  increased BUN and creatinine levels  electrolyte imbalance Immunoglobulin A Nephropathy  AKABerger Disease, IgA nephropathy: immune complexes containing IgA are deposited on the glomerular membrane.  most common cause of glomerulonephritis  Increased levels of serum IgA, may be a result of mucosal infection  most frequently seen in children and young adults Immunoglobulin A Nephropathy - Lab findings  Macroscopichematuria after an infection or strenuous exercise  Asymptomatic microhematuria  Elevated serum levels of IgA  Gradual progression to chronic glomerulonephritis and ESRD Nephrotic Syndrome  marked by massive proteinuria (greater than 3.5 g/day)  low levels of serum albumin  high levels of serum lipids  pronounced edema