Ricca Christyl O.

Sumalpong MT35-CD

Activity on Renal Diseases

Renal Diseases Etiology Urinalysis Findings % that progress to

chronicity
Glomerular disorders:
Glomerulonephritis
Acute glomerulonephritis Deposition of immune complexes on the Macroscopic hematuria Nearly all
glomerular membrane, formed in association Proteinuria
with group A Streptococcus infection RBC cast
Granular Cast
Rapidly progressive Deposition of immune complexes from Macroscopic hematuria Mostly to do not develop
glomerulonephritis systemic immune disorders on the glomerular RBC casts chronicity because
membrane Proteinuria disease progression is
rapid
Goodpasture syndrome Attachment of cytotoxic antibody formed Macroscopic hematuria Commonly progresses to
during viral respiratory infections to Proteinuria chronic
glomerular and alveolar basement membranes RBC casts glomerulonephritis and
end-stage renal failure
Wegener granulomatosis Anti-neutrophilic cytoplasmic autoantibody Macroscopic hematuria
binds to neutrophils in vascular walls Proteinuria
producing damage to small vessels in the lungs RBC casts
and glomerulus.
Henoch-Schonlein purpura Occurs primarily in children following viral Macroscopic hematuria
respiratory infections; a decrease in platelets Proteinuria
disrupts vascular integrity RBC casts
Membranous Thickening of glomerular membrane following Hematuria 20-30%
glomerulonephritis IgG immune complex deposition associated Proteinuria
with systemic disorders
Membranoproliferative Cellular proliferation affecting the capillary Microscopic hematuria uncommon
glomerulonephritis walls or the glomerular basement membrane, Proteinuria
possible immune-related
 Chronic glomerulonephritis
IgA nephropathy (early stages)
IgA nephropathy (late stages)
Nephrotic Syndrome
Minimal change disease
Focal Segmental
glomerulosclerosis
Alport syndrome
Diabetic nephropathy (late
stages)
Tubular disorders
Marked decrease in renal function resulting Hematuria
from glomerular damage precipitated by other Proteinuria
renal disorders Glucosuria
Cellular and granular casts
Waxy and broad casts
Deposition of IgA on the glomerular Macroscopic or microscopic
membrane resulting from increased levels of hematuria
serum IgA *Similar with chronic
glomerulonephritis
Disruption of the shield of negativity and Heavy proteinuria 1/3 progresses to toward
damage to the tightly fitting podocyte barrier Microscopic hematuria end-stage renal disease
resulting in massive loss of protein and lipids Renal tubular cells
Oval fat bodies
Fat droplets
Fatty and waxy casts
Disruption of the podocytes occurring Heavy proteinuria 2.9% progresses to
primarily in children following allergic Transient hematuria chronicity with those
reactions and immunizations Fat droplets whose CD80 levels
above 328.98 ng/g
creatinine
Disruption of podocytes in certain areas of Proteinuria
glomeruli associated with heroin and analgesic Microscopic or macroscopic
abuse and AIDS hematuria
Genetic disorder showing lamellated and *early stages is similar with
thinning glomerular basement membrane nephrotic syndrome
Late stages is added with
microalbumiuria
Glomerular membrane damage occurs as a *Similar with chronic 30-40%
result of glomerular membrane thickening and glomerulonephritis
increased proliferation of cellular and non-
cellular matrix in the glomerular matrix
Acute tubular necrosis
Hereditary and Metabolic
Tubular disorders
Fanconi syndrome
Alport Syndrome
Uromodulin Associated Kidney
Disease
Diabetic nephropathy
Nephrogenic Diabetes insipidus
Renal glycosuria
Interstitial Disorders
Cystitis
Acute pyelonephritis
Damage to tubular cells caused by ischemia or Microscopic hematuria 20%
toxic agents Proteinuria
Renal tubular epithelial cells
Renal tubular epithelial cell
casts
Hyaline, granular, waxy,
broad casts
Inherited in association with cystinosis and Glucosuria In very rare instances a
Hartnup disease or acquired through exposure Possible cystine crystals patient who have
to toxic antigens idiopathic Fanconi’s
syndrome progresses to
chronic renal failure.
Genetic disorder showing lamellated and Renal tubular epithelial cells
thinning glomerular basement membrane
Inherited defect in the production of normal
uromodulin by the renal tubules and increased
uric acid causing gout.
Deposition of glycosylated proteins resulting Glucosuria 20-40%
from poorly controlled blood glucose levels
Inherited defect of tubular response to ADH or Low specific gravity, polyuria
acquired from medications
Inherited autosomal recessive trait Glucosuria
Ascending bacterial infection of the bladder Leukocyturia
Bacteriuria
Microscopic hematuria
Mild proteinuria
Increased pH
Infection of the renal tubules and interstitium Leukocyturia
related to the interference of urine flow to the Bacteriuria
WBC casts
 bladder, reflux of urine from the bladder and Bacterial casts
untreated cystitis Microscopic hematuria
Proteinuria
Chronic pyelonephritis Recurrent infection of the renal tubules and Leukocyturia
interstitium caused by structural abnormalities Bacteriuria
affecting the flow of urine WBC casts
Bacterial casts
Granular, waxy, broad casts
Hematuria
Proteinuria
Acute Interstitial Nephritis Allergic inflammation of the renal interstitium Hematuria A small portion of drug
in response to certain medications Proteinuria induced AIN progress to
Leukocyturia endstage chronic kidney
WBC casts disease
Renal Failure
Prerenal Decreased blood pressure/cardiac output Varied urinalysis findings but
Hemorrhage some specific findings
Burns include the following:
Surgery • RTE cells and casts- ATN
Septicemia of prerenal origin
Renal Acute glomerulonephritis • RBCs- glomerular injury
Acute tubular necrosis • WBC casts with or
Acute pyelonephritis without bacteria-
Acute interstitial nephritis interstitial infection or
Post renal Renal calculi inflammation or renal
Tumors origin
Renal Lithiasis
Renal lithiasis pH changes, chemical concentration, and Calcium oxalate crystals
urinary stasis Calcium phosphate crystals
Increased intake of foods with high purine Microscopic hematuria
content and with uromodulin-associated
kidney disease
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