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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

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