Critical Care Nursing

Renal Outline: Pathophysiologies

Critical Care Nursing, The University of Iowa
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IV. Pathophysiologies

80,000 - 110,000 die per year due to renal problems. 1.2 million conditions requiring hospitalization are related to renal stones, UTIs and other conditions.

Medicare covers 95% of dialysis and transplants.

A. Congenital defects

10% of persons born have potentially significant malformations of the urinary system.

1. Unilateral agenesis - relatively common; people often unaware.
2. Agenesis - Incompatible with life; infants usually stillborn.
3. Hypoplasia - Kidneys are not normal size; often only affects 1 kidney. If both, it progresses to renal failure, dialysis, and/or death.
4. Horseshoe kidney - Fusion of the kidneys at the midline. Usually no problem.
5. Dysplasia - Most common; i.e.: multicystic kidney, atresia or obstruction of the ureter.
6. Polycystic disease - Inherited; requires interventions such as surgery, drug therapy, transplant, and dialysis.

B. Urinary Tract Infections (UTIs)

Second most common type of infection (Respiratory is first). 20% of all women will have one in their lifetime.

1. Bacteriuria. Presence of 100,000 or more organisms per ml of urine. Common complication associated with the use of foley catheters. CDC recommends that patients with a foley catheter not share a room.
2. Cystitis. Infection of the bladder. Characterized by frequency, urgency, lower abdominal discomfort, and dysuria.
3. Pyelonephritis. Inflammed areas of the kidney and renal pelvis. Can develop scar tissue. Patient is usually very ill: symptoms inlcude pain and chills, decrease in renal function.
4. Chronic Pyelonephritis. Characterized by scarring an deformation. May lead to loss of tubular function. May have severe hypertension which contributes to a significant cause of renal failure.

   a. Treatments

   1. Sulfonamides
   2. Fluids

C. Obstructive Disorders

1. Hydronephrosis. Dilatation of the renal pelvis with renal atrophy. Causes interference with blood flow and glomerular filtration. If obstruction continues, permanent damage occurs in 3 weeks.
2. Urolithiasis (stones). One-third of people with recurrent stones will lose a kidney.

a. Types
1. Staghorn - fills renal pelvis
2. Calcium (oxalate or Phosphate) make up 80-90% of stones
3. Magnesium ammonium phosphate bacteria causes splitting of urea then stone forms.
4. Uric acid - found in people with gout
5. Cystine - rare and genetic in cause.

D. Glomerulonephritis

Most common following infections by strains of group A, beta-hemolytic streptococci. In this situation, there is an abnormal immune reaction, causing immune complexes to become entrapped in the glomerular membrane, inciting an inflammatory response. The capillary membrane swells and is then permeable to plasma proteins and blood cells. Usually follows a strep infection by 10 days to 2 weeks (the time needed for formation of antibodies). Oliguria is an early symptom, Na and H20 retention causes edema, particularly of the face and hands, along with hypertension. Proteinuria and hematuria follow from the increased capillary permeability. This may give a smoky hue to the urine ("cola" colored).

E. Diabetic glomerulosclerosis

Most important manifestation of diabetic neuropathy. Diffuse type - thickening of basement membrane. Nodular type - (Kimmelstiel-Wilson syndrome) hyaline deposits on the glomerulus. Both types present with proteinuria, with a slow, steady progression to renal failure.

F. Acute Renal Failure (ARF)

Is a potentially reversible condition that results in acute suppression of renal function. Acute renal failure may rapidly present a life threatening situation which is amenable to appropriate medical management provided that the situation is recognized. Evidence of renal involvement may be masked by the primary medical, surgical, or obstetric condition.

 
• 1. Pathogenesis

  The pathogenesis remains controversial and inconclusive but the theories most often encountered include bakleak, tubular, obstruction, vascular obstruction, and reninangiotensin. Regardless of the pathoensis, pathologic studies have described two characteristic histologic insults:

  1. Iscemia
     This tends to produce pathcy lesions affecting the proximal and distal tubular segments. The basement cell membrane is disrupted and tubular necrosisis present
  2. Nephrotic
     This usually leaves the basement membrane intact while tubular destruction can range from simple cellular swelling to frank necrosis. Damage is seenprimarily in the proximal tubulaar segments. The influences that may bear on kidney function sare usually considered in terms of three separate but requently interrelated categories.

  2. Categories of ARF

   
  • a. Prerenal

    Prerenal causes of renal failure act by reducing glomerular perfusion either by vasoconstriction, or a reduction of mean arterial pressure. This may e due to locl or general causes:

     
    • i. Local
      • -embolism or thrombosis
      • -surgical operation
      • -hepatorenal syndrome

       

    • ii. General
      • -hypovolemia due to hemorrhage, burns, cardiac insufficiency GI losses
      • -peripheral vasodilators associated with excessive anihypertensivetherapy
      • -bacteremic shock

    Many of these conditions can occur in the presence of a normal blood pressure and go undetected until renal symptons present.

    Frequent consideration of the clinical situation will help assist in identifying prerenal causes for ARF.

     
  • b. Renal (or intrarenal)

    Renal causes of ARF are due to parenchymal changes resulting from disease or nephrotoxic agents that induce renal disease.

    Diseases of the renal parenchyma other than ischemia account for 25% of all cases of ARF. These include glomerular lesions such as acute poststreptococcal glomerulonephritis, SLE, papillary necrosis, and vasculitides (polyarteritis nodosa), Goodpasture's, Wegener's, and malignant hypertension.

    Can be grouped into 5 categories:

    1. Ischemia - occurs when perfusion to the kidney is obliterated or reduced below a mean systemic blood pressure of 60-70 mmHg in the afferent arteriole.
    2. Injury to the glomerular membrane (acute glomerulonephritis)
    3. Acute tubular necrosis (ATN) characterized by destructive changes in the tubular epithelium due to ischemia or exposure to nephrotoxic agents. Shock and heart failure, for example, cause prerenal failure, tend to cause renal ischemia, and if allowed to progress, can produce tubular necrosis. As a rule, the blood supply to a normal kidney can be interrupted for about 30 minutes without inflicting damage to the kidney. Trauma, sepsis, and heart failure may interrupt blood flow for a longer duration.
       Nephrotoxic drugs may be ingested, inhaled therapeutically, accidentally, or with suicidal intent. Widespread use of nephrotoxic antibiotics has contributed to a high frequency of ATN. The sulfonamides, methicillin and cephalosporins, along with aminoglycosides such as gentamicin, tobramycin, vancomycin, and amikacin are some of the most common nephrotoxic antibiotics. The aminoglycosides bind avidly to proximal tubular epithelial cells with a half life of 109 hours (5 1/2 days).
       Radiologic contrast media can also produce tubular damage. Radiographic dye usually promotes an osmotic diuresis and urine losses of up to 7 ml for every 1 ml of dye used.
    4. Intratubular obstructions - due to accumulation of casts and cellular debris, secondary to severe hemolytic reactions or myoglobinuria. Skeletal and cardiac muscle contains myoglobin, which accounts for their rubiginous color. Myoglobin corresponds to hemoglobin in function, serving as an oxygen reservoir within the muscle fibers. Myoglobin is not normally found in the serum or urine. It has a low molecular weight, so should it escape into the circulation, it is rapidly filtered in the glomerulus. Myoglobinuria is most commonly due to muscle trauma, but may result from extreme exertion, hyperthermia, sepsis, prolonged seizures, potassium or phosphate depletion, alcoholism or drug abuse. Can be traumatic or non-traumatic. Hemoglobin may also escape into the glomerular filtrate due to severe hemolytic reaction. Both myoglobin and hemoglobin cause discoloration of the urine, ranging from the color of tea to red, brown, or black.
    5. Acute pyelonephritis or necrotizing papillitis - bacterial infection of the kidney and renal pelvis.
     
  • c. Postrenal

    Postrenal causes of ARF are due to urinary tract obstruction, secondary either to structural or fuctional lesions of the urinary passages. The obstruction may occur anywhere from the tubules to the kidneys to the external urethral orifice. The cause may vary from stricture through stone to tumors of the urinary passages or of adjacent pelvic or abdominal organs.

    Functional obstruction may follow the use of drugs which interfere with the autonomic supply to bladder or urinary passages such as ganglion blockage or antihistamines.

    With diabetes mellitus the advent of an imbalance in the neurogenic supply may be sufficient to disturb the equilibrium and precipitate the obstruction.

    Amuria associated with ARF is usually indicative of a post renal cause.

G. Chronic Renal Failure (CRF)

A slow, progressive renal disorder culminating in end stage renal disease (ESRD). The decline in kidney function correlated with the degree of nephron loss.

 
• 1. Pathophysiology.
  Systemic changes occur when overall renal function is less than 20-25% of normal.
  • a. Bricker's "intact nephron" hypothesis provides an explanation for the kidney's ability to compensate and preserve homeostasis despite a significant loss of 80% of nephron function.

    During CRF, regardless of etiology, injury occurs to the nephrons in a progressive manner. Significant damage to groups of nephrons will eliminate them from their contributing role in maintaining renal function. The remaining intact nephrons will compensate by experiencing cellular hypertrophy. This growth process will enable them to accept larger blood volumes for clearances resulting in the exertion of greater solute levels, thus compensation results.

  • b. Stages of CRF
    • i. Diminished renal reserve
      • 50% nephron loss
      • --Kidney function is mildly reduced while the excretory and regulatory function are sufficiently maintained to preserve a normal internal environment. The patient is usually problem free.
      • --The patient's normal serum creatinine will double.
    • ii. Renal insufficiency
      • 75% nephron loss
      • --Evidence of impaired renal capacity that appears in the form of mild azotemia, slightly impaired urinary concentrating ability, and anemia.
      • --Factors that can exacerbate the disease at this stage by increasing nephron damage are: infection, dehydration, drugs and cardiac failure.
    • iii. End Stage Renal Disease (ESRD)
      • 90% of the nephrons are damaged
      • --Renal function has so deteriorated that chronic and persistent abnormalities exist in the internal environment.
      • --Patient requires artificial support to sustain life, i.e. dialysis, transplant
    • iv. Uremic Syndrome
      • --The body's systemic responses to the buildup of uremic waste products and the results of the failed organ system.
      • --Usually described as the constellation of signs and symptoms demonstrated by the RF patient.
      • --Symptoms may be avoided or diminished by initiation of early dialysis treatment.

H. LUPUS NEPHRITIS

Is the cause of approximately 3% of cases of ESRF (end-stage renal failure) requiring maintenance dialysis or transplantation. It is characterized by deposits of immune reactants in different sites along the nephron. There are many different forms of lupus nephritis each with its own characteristics. Treatment is based on the severity and progression of the disease. Many tests are used to follow the course of acute episodes and are used as a guideline to therapy. No one test is specific enough to be used individually.

Treatment includes: corticosteroids, cytotoxic drugs, plasma exchange therapy, Cyclosporine A, and pulse methylprednisone. Presenting symptoms include: proteinuira and hematuria.

J. GOODPASTURE'S

Is a syndrome consisting of pulmonary hemorrhages and glomerulonephritis of primary crescentic type. Frequently the term Goodpasture's is used in a purely clinical sense without reference to pathology or immunopathology.

The disease is most common in young adult males but occurs at any age.

The onset is sometimes preceded by "flu-like" symptoms.

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Last Modified: January 22, 1997