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patho week 5

chapter 27 & 28
Renal pain
(nephralgia) generally felt at costovertebral angle
spinal cord between T10 and L1 by sympathetic afferent neurons; may be felt throughout dermatomes of T10-L1
Abnormal Urinalysis Findings
foundation for the differential diagnosis of renal dysfunction
identifies gross abnormalities related to size, position, and shape (may show renal calculi)
Renogram/renal scan
shows renal vasculature
differentiates tissue characteristics
provide detailed information about the vasculature and tissue
Renal Agenesis and Hypoplasia
Unilateral renal agenesis results in compensatory hypertrophy of functional kidney
Cystic Kidney Diseases
Genetically transmitted renal disorder resulting in cysts that can expand and disrupt urine formation and flow; may be localized to one area or affect both kidneys
Autosomal recessive
are evident at birth
Autosomal dominant
symptoms later in life (adult) with 50% chance of developing the disease in offspring.
Benign Renal Neoplasms
Symptoms depend on the size; may be asymptomatic until large enough to form palpable abdominal mass, hematuria, and flank pain
treatment of choice for Benign Renal Neoplasms
Renal Cell Carcinoma
Usually asymptomatic until advanced; presenting S/S include CVA tenderness, hematuria, palpable mass,
May have familial pattern
smoking and obesity
Risk factors for Renal Cell Carcinoma
Nephroblastoma (Wilms Tumor
Most common kidney cancer in children
Identified by palpable abdominal mass; may also have pain, hypertension, and/or hematuria
Acute Pyelonephritis
Infection of renal pelvis and parenchyma usually due to an ascending urinary tract infection
The most common agent associated with the Acute Pyelonephritis
Presence of WBC casts
is indicative of upper UTI
to avoid decreased renal function of Acute Pyelonephritis
symptoms of Acute Pyelonephritis
CVA tenderness a classic sign Accompanied by fever, chills, N/V, anorexia
Chronic Pyelonephritis
Usually associated with vesicoureteral reflux or obstructive process leading to persistent urine stasis
Ongoing inflammation (Chronic Pyelonephritis)
causes fibrosis and scarring and loss of functional nephrons
Renal Calculi (Nephrolithiasis)
Obstructive processes result in urine stasis, predisposing to infection and structural damage
common causes of Renal Calculi
stones, tumors, prostatic hypertrophy, and strictures of the ureters or urethra
what is the most common cause of Renal Calculi?
Renal stones
Complete obstruction (Renal Calculi)
leads to hydronephrosis, decreased GFR, and ischemic damage due to increased intraluminal pressure
Prolonged postrenal ARF
may result in ATN and CKD
Stones tend to form in urinary tract
due to solute supersaturation, low urine volume, and abnormal urine pH
calcium crystals
Most stones are composed of
composition of other stones
uric acid (in gout), struvite, cystine, and stones associated with certain medications
Uric acid stones
are radiolucent and therefore are not detectable by plain x-ray
Stationary stones
usually asymptomatic; stone migration causes intense renal colic pain abrupt in onset and may radiate; N/V, diaphoresis is commo
Colicky, spasmodic pain in the flank area
is likely to occur with ureteral irritation.
lithotripsy or endoscopic approaches
common interventions for stones
alter glomerular capillary structure and function
mediated by immune processes
damage to glomerular capillary structure
presence of red blood cell casts
in the urine is indicative of glomerulonephritis.
some results of glomerulopathies
some combination of hematuria, proteinuria, abnormal casts, decreased GFR, edema, and hypertension
Immune response to variety of potential triggers; may have primary or secondary etiology
What causes the GFR to fall?
contraction of mesangial cells resulting in decreased surface area for filtration
Treatments for Glomerulonephritis
steroids, plasmapheresis, and supportive measures such as dietary and fluid management
ESRD (end-stage renal disease)
common outcome of chronic glomerulonephritis; dialysis or kidney transplantation may be necessary,
end-stage renal disease
chronic kidney disease, a condition which serum creatine and BUN levels rise and may result in impairment of all body systems
Nephrotic Syndrome
Occurs due to increased glomerular permeability to proteins
3 to 3.5 g of protein per day
Urinary loss of proteins in Nephrotic Syndrome
leads to
a.) hypoalbuminemia and generalized edema
b.) decreased blood colloid osmotic pressure
c.) increase in liver activity can cause hyperlipidemia and hypercoagulability
frequently used synonymously with nephrotic syndrom, with less proteinuria (<2 gram a day)
ARF (acute renal failure)
an abrupt reduction in renal function producing an accumulation of waste materials in the blood,
serum creatinine and creatinine clearance
bsis for monitoring Renal function
Retention of metabolic wastes
Patients with ARF
commonly develop metabolic acidosis because of impaired kidney secretion of H+.
Prerenal Acute Renal Failure
Due to conditions that impair renal blood flow, such as hypovolemia, hypotension, hypertension, cardiac failure, renal artery obstruction, nephrosclerosis and renal artery stenosis.
characteristics of Prerenal Acute Renal Failure
a.) low GFR,
b.) oliguria,
c.) high urine specific gravity and osmolality, and
d.) low urine sodium
Prolonged prerenal ARF
leads to intrarenal RF
Postrenal Acute Renal Failure
Due to obstruction within the urinary collecting system distal to the kidney; elevated pressure in Bowman capsule; impedes glomerular filtration
Intrarenal Acute Renal Failure
Due to a primary dysfunction of the nephrons
Most often due to problem within the renal tubules resulting in acute tubular necrosis; may also occur with glomerular, vascular, or interstitial etiologies
Clinical Presentation of Acute Tubular
Necrosis: Oliguric Stage
Characterized by
a.) oliguria and progressive uremia;
b.) decreased GFR;
c.) hypervolemia
May last 1 to 2 weeks
Glomerular Filtration Rate
The best indicator of renal function
serum creatinin.
The most helpful lab value in monitoring the progression of declining renal function
Clinical Presentation of Acute Tubular
Necrosis: Diuretic Stage
Urine volume increases, but tubular function remains impaired and azotemia continues
May last 2 to 10 days
Clinical Presentation of Acute Tubular
Necrosis: Recovery Stage
Characterized by gradual normalization of serum creatinine and BUN
May last up to 12 months
Often a degree of renal insufficiency
Chronic Kidney Disease
Outcome of the progressive and irrevocable loss of nephrons; a global health problem often linked with other comorbidities, primarily hypertension and DM
Chronic Kidney Disease defined as
decreased kidney function or kidney damage of 3 months' duration based on blood tests, urinalysis, and imaging studies; GFR <60 ml/minute/1.73 m2 for 3 months with or without indication of damage to the kidney
risk factors for CKD
Most commonly associated with DM, hypertension, recurrent pyelonephritis, glomerulonephritis, and polycystic kidney disease
CKD causes the following:
a.) alterations in glomerular perfusion and filtration,
b.)sodium reabsorption,
c.) renal sympathetic activity, and
d.) activity of the RAAS
Pathophysiology of Progression of
Chronic Kidney Disease
Glomerulosclerosis and interstitial inflammation and fibrosis
Monitored by two staging systems
Percentage of nephron loss
Reduction in GFR
GFR reduction occurs with nephron loss
Stages of Chronic Kidney Disease
Defined by level of function per GFR
Decreased renal reserve is not associated with S/S of renal failure; interventions required to slow disease progression
Renal insufficiency characterized by increase in metabolic wastes at levels proportional to nephron loss; polyuria
Complications of Chronic Kidney Disease
a.) Hypertension and cardiovascular disease
b.) Uremic syndrome
c.) Metabolic acidosis
d.) Electrolyte Imbalances
e.) Renal osteodystrophy
f.) Malnutrition
g.) Anemia
Hypertension and cardiovascular disease
due to hypervolemia, escalated atherosclerotic process, heightened RAAS activity, and increased SNS activity
Uremic syndrome
due to retention of metabolic wastes
Metabolic acidosis
due to retention of acidic waste products; kidneys lose ability to secrete H+ ions and bicarbonate
Electrolyte Imbalances
retention of potassium, phosphorus, and magnesium in the blood
Renal osteodystrophy
elevated PTH causes altered bone and mineral metabolism; kidneys unable to reabsorb calcium and insufficient active vitamin D
patients with ESRD are at a high risk of developing
decreased intake due to uremic syndrome, depression, dietary limitations, and changes in taste
due to lack of erythropoietin
Primary foci
are appropriate management of ATN, blood glucose control in diabetes, ACE inhibitors or AII blockers to reduce proteinuria, and aggressive management of hypertension and cardiovascular disease
Nutritional needs for patients with CKD
include increased calories, calcium, and vitamin supplementation
Nutritional restrictions for patients with CKD
Fluids, phosphorus, potassium, sodium, and protein intake
Drug therapy for CKD
used to control hypertension, anemia, and some of the electrolyte imbalances