Class notes
Path 370 Intrarenal Disorders Notes
- Course
- PATH 370
- Institution
- West Coast University
This is a comprehensive and detailed note on Intrarenal disorders for Path 370. *Essential!! *For you!!
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WK6 Objectives:Chapter 27 Intrarenal Disorders
Occur primarily within the kidney and have the potential to result in renal insufficiency or failure
Categories
Congenital-could be a genetic disorder
Neoplastic-malignant, could be because of bacteria
Infectious-infected
Obstructive-obstructive urinary tract
Glomerular
Common Manifestations of Kidney Disease
Pain
Kidney and renal pain: nephralgia (pain) in the back. Pain receptors are in the capsule.
Generally felt at costovertebral angle; recorded as CVA tenderness or flank pain
Due to distention/inflammation of the renal capsule; has a dull, constant character
Pain transmitted to T10 and L1 by sympathetic afferent neurons; may be felt throughout dermatomes (area of skin innervated by a specific
spinal cord segment)
Abnormal Urinalysis Findings
Dipstick and microscopic urinalysis results provide clues to intrarenal pathologies
Color
Dark, strong-smelling urine: decreased renal function
Cloudy pungent urine: infectious process
Other Diagnostic Tests/Imaging Tests
KUB (Kidney, ureter, bladder test) identifies gross abnormalities related to size, position, and shape (may show renal calculi)
Renogram/renal scan shows renal vasculature and tumors
Ultrasonography differentiates tissue characteristics
CT/MRI used to provide detailed information about the vasculature and tissue
Congenital Abnormalities
Renal Agenesis and Hypoplasia
Agenesis: kidneys do not develop in the fetus
Bilateral agenesis not compatible with life
Unilateral agenesis compensatory hypertrophy of functional kidney
Hypoplasia: some fetal kidney development
Can lead to pediatric end-stage renal failure
A single normal kidney can maintain normal renal function
Requires lifelong kidney monitoring
Cystic Kidney Diseases
Genetically transmitted renal disorder resulting in fluid-filled cysts that can expand and disrupt urine formation and flow; may be localized
to one area or affect both kidneys
Can lead to renal failure, requiring dialysis or transplantation at late stage
2 types***
Autosomal recessive forms—at birth
Autosomal dominant types—later in life
Neoplasms
Renal Cell Carcinoma
Metastatic disease
May have familial pattern; risk factors (smoking, obesity, hypertension)
Asymptomatic until advanced
CVA tenderness, hematuria, palpable mass
Staging system: I-IV
Treatment: nephrectomy
Metastases may be particularly resistant to radiation, immunotherapy, and chemotherapy (p53 mutation)
Nephroblastoma (Wilms Tumor)
Most common kidney cancer in children
Clinical manifestations: identified by palpable abdominal mass; may also have abdominal pain, hypertension, and/or hematuria
Treatment: nephrectomy, radiation therapy, and chemotherapy
1
, Excellent cure rate
Infection
Infection of the kidney: pyelonephritis (what would be the expected S/S in clinic?)
Most common: ascending infection from the lower urinary tract
Most effective preventive measure: early removal of catheters
Infection
Acute Pyelonephritis
Infection of renal pelvis/parenchyma usually from ascending UTI
Clinical manifestations: CVA tenderness (classic sign) accompanied by fever, chills, N/V, anorexia, which increases fever-induced
dehydration
Diagnosis: presence of WBC casts indicative of upper UTI
Treatment: promptly managed with antimicrobials to avoid decreased renal function
Obstruction
Conditions that interfere with the flow of urine
Obstructive processes cause
Urine stasis: Predisposes to infection and structural damage
Common causes
Stones: most common (composed of calcium crystals; others include uric acid, struvite, cystine)
Tumors
Prostatic hypertrophy
Strictures of the ureters or urethra
Complete obstruction results in ****
Hydronephrosis
Decreased GFR
Ischemic kidney damage because of increased intraluminal pressure
Acute tubular necrosis (intrarenal acute renal failure)—self-limiting disorder
Chronic kidney disease
Glomerular Disorders
Acute Glomerulonephritis
Immune response to variety of potential triggers***
Attraction of immune cells to the area of inflammation results in lysosomal degradation of the basement membrane
GFR may fall due to contraction of mesangial cells resulting in decreased surface area for filtration
Clinical manifestations****: Proteinuria, oliguria and azotemia, edema and hypertension
Treatment
Steroids
Plasmapheresis
Supportive measures such as dietary and fluid management
Management of systemic and renal hypertension
Chronic Glomerulonephritis
Assumes a progressive course ultimately developing into end-stage renal disease
Sclerosis and fibrosis of kidney**
Present with persistent proteinuria, with or without hematuria, and slowly declining renal function**
Supportive interventions throughout course of disease
Dialysis or kidney transplantation necessary
Nephrotic Syndrome****
Occurs due to increased glomerular permeability to proteins
Urinary loss of 3 to 3.5 g of protein per day
Proteinuria leads to hypoalbuminemia and generalized edema; decreased blood colloid osmotic pressure
Increase in liver activity can cause hyperlipidemia and hypercoagulability
Most common finding: edema
Treatment: conservative symptom management
Diuretics
Lipid-lowering agents
Antihypertensives
2
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