AUB - Renal Diseases

RENAL DISEASES CLASSIFICATION OF RENAL DISEASES 1. Glomerular Disorder 2. Tubular Disorder 3. Interstitial Disorder GLOMERULAR DISORDER  Usually of immune origins that results to immunologic disorders.  Increased production/ circulation of Ig. (especially IgA)  Deposition of immune complexes in glomerular membrane. (e.g. amyloidosis) GLOMERULONEPHRITIS  Refers to sterile inflammatory processes that affects the glomerulus and associated with the finding f blood, protein and casts in urine. 1.

It is CAUSED by:  Certain strains on Group A Streptococcus (Streptococcus pyogenes)  Pneumonia  Endocarditis  Severe infection FINDINGS: a) Hematuria b) Protienuria c) Oliguria d) Presence of casts (RBC cast, WBC casts, Hyaline Casts, Granular Casts) e) Increased BUN Levels f) POSITIVE ASO Titer 2.

Rapidly Progressive (Crescentic) Glomerulonephritis  More serious form which can definitely lead to renal failure.  Has poor prognosis  Damage to capillary wall is due to macrophages that will release cells and plasma in the Bowman’s space.  Production of crescentic formations containing macrophage, fibroblast and polymerized fibrin.

3.

Goodpasture Syndrome  Due to the cytotoxic antibody (Antiglomerular Basement membrane) found attached to the glomerular and alveolar membranes during viral respiratory infection.  Autoantibody attachment and complement activation causes the damage to the capillaries.  Patient’s initial complaints are hemoptysis & dyspnea followed by the development of hematuria.

4.

Vasculitis  Disorders affecting the systemic vascular system resulting to the glomerular damage.  These disorders are immune mediated.

B.

Henoch- Schönlein Purpura Result of allergic vasculitis which invloves the skin, GIT, kidneys, heart and CNS. It is considered as an immune complex disease and is characterized by involvement of capillaries with diffuse infiltration of neutrophils, lypmhocytes and macrophages. It is commonly seen in children; renal dysfunction is common and is the most serious complication. Typically reversible in children.

Immunoglobulin A Nephropathy/ Berger’s Disease  Frequently seen in children and young adults.  Immune complexes are deposited on the glomerular membrane.  Patient’s serum IgA level is increased which may result from mucosal infection.  Patient may remain asymptomatic for 20 years may there is a gradual progression to chronic glomerulonephritis and end stage renal disease.

6.

Membranous Glomerulonephritis  Thickening of the glomerular membrane due to deposition of IgG immune complexes.  Thombosis may develop.  Nephrotic Syndrome occurs.

SYMPTOMS: Hypertension Oliguria Hematuria

Wegener’s Granulomatosis causes granuloma producing inflammation of the small blood vessels in the lungs and the kidneys. caused by antineutophilic cytoplasmic antibody (ANCA), which can be demonstrated in patient’s serum for laboratory testing.

5.

Acute Poststreptococcal Glomerulonephritis  Sudden onset of symptoms with consistent damage to the glomerular membrane.

Fever Edema Fatgiue

A.

DISORDERS ASSOCIATED: a) Systemic Lupus Erythematosus (SLE) b) Sjögren Syndrome - a chronic progressive inflammatory autoimmune disorder characterized by marked excessive drying of mouth and eyes from exocrine disorder and B cell lymphoproliferative disorder. c) Secondary syphillis d) Hepatitis B e) Gold & mercury treatment f) Malignancy 7.

Membranoproliferative Glomerulonephitis  Immune mediated disorder mostly affecting children characterized by cellular proliferation in capillary walls or glomerular basement membrane. a) Type I Increased cellularity in the subendothelial cells of the interstitial area of the Bowman’s capsule, causing thickening of the capillary walls; progress to nephrotic syndrome b) Type II Extreme dense deposits in the glomerular membrane Experience symptoms of chronic glomerulonephritis.

8.

Chronic Glomerulonephritis  Glomerular damage as a result of renal disorder leads to marked decreased in renal functions and eventually to renal failure.

9.

Nephrotic Syndrome  There s increase permeability of the glomerular membrane due to disruption in the electrical charges in the basal lamina and podocytes, producing a less tightly connected barrier that allows massive loss of protein and lipids.  Characterized by the presence of RTE cells, RTE cell casts, & fatty casts.

10. Minimal Change Disease (Lipid Nephrosis)  Podocytes appear to be less tightly fitting allowing increase infiltration of protein.  Seen in children following allergic reaction and immunization. 11. Focal Segmental Glomerulosclerosis  Only a certain number and areas of the glomerulus are affected.  The disease is caused by the disruption of podocytes associated with analgesic and heroin abuse and AIDS.  IgM and C3 are seen in the undamaged glomerulus. 12. Alport Syndrome  An inherited disorder affecting the glomerular basement membrane.  Inherited as a sex-linked or autosomal genetic disorder.  Males are frequently more severely affected than females.  Glomerular basement membrane has a lamellated appearance with areas of thinning.  Prognosis ranges from mild symptoms to persistent hematuria and renal insufficiency in later life to the nephrotic syndrome and end-stage renal disease. 13. Diabetic Nephropathy  also known as Kimmelstiel-Wilson disease  Currently the most common cause of end-stage renal disease.  Increased proliferation of mesangial cells and increased deposition of cellular and noncellular material within the glomerular matrix resulting in accumulation of solid substances around the capillary tufts.  Microalbumin monitoring in DM patients is important to detect the onset of Diabetic Nephropathy. TUBULAR DISORDER Acute Tubular Necrosis  primary disorder associated with damage to the renal tubules  RTE cells are damaged by toxic agents (aminoglycosides, amphotericin, cyclosporine, radiographic dyes, ethylene glycol, mushroom poisoning, heavy metals) or ischemia (shock, trauma caused by crushing injuries and surgical procedures.) Hereditary and Metabolic Disorder 1.

2.

Fanconi’s Syndrome (Hereditary) disorder most frequently associated with tubular dysfunction May be inherited in association with cystinosis and Hartnup’s Disease. Acquired Associated with exposure to toxic agents.

INTERSTITIAL DISORDER  Disorders affecting the renal interstitium which also affects the tubules (tubulointerstitial diease)  Involves inflammatory conditions and infections. a.

Cystitis  Ascending bacterial infection of the bladder

b.

Acute Pyelonephritis  Infection of the upper urinary tract involving the interstitium and tubules due to interference of urine flow to the bladder, reflux of urine from the bladder untreated cystitis

c.

d.

Chronic Pyelonephritis  Recurrent infection of the tubules and interstitium caused by structural abnormalities affecting urine flow (congenital) Acute Interstitial Nephritis  Inflammation of the renal interstitium associated with allergic reaction to medications.

RENAL FAILURE Chronic Renal Failure Characterized by:  Decreased glomerular filtration rate (GFR)  Azotemia (increased BUN and serum creatinine levels)  Electrolyte imbalance  Lack of renal concentrating activity  Proteinuria  Renal glycosuria  Presence of telescoped sediments (waxy, broad & granular casts) Acute Renal Failure CAUSES: 1. Prerenal causes  Burns  Hemorrhage  Surgery 2. Renal Causes  Acute glomerulonephritis  Acute pyelonephritis  Acute tubular necrosis 3. Postrenal causes  Tumors  Calculi  Crystallization of ingested substancces GENERAL CHARACTERISTICS OF ACUTE RENAL FAILURE:  Decrease in GFR  Oliguria  Edema  Azotemia RENAL LITHIASIS  Deposition of renal calculi or kidney stones in the calyces and pelvis of the kidney, ureters and urinary bladder. CONDITIONS FAVORING STONE FOMATION:  pH  Chemical concentration  Urinary stasis CHEMICAL COMPOSITION OF RENAL CALCULI:  Calcium oxalate or phosphate  Magnesium ammonium phosphate  Uric acid  Cystine PATIENT MANAGEMENT:  Maintaining the urine at a pH incompatible with crystallization of the particular chemicals  Maintaining adequate dehydration to lower chemical concentration  Dietary restrictions