1. Management of Patients with alterations in the Renal system
C. Cummings RN, EdD

2. Renal Anatomy

3. Anatomy System includes the kidneys and entire urinary tract
2 kidneys located behind the peritoneum, on either side of the spine
Weighs about 8 oz and the left if longer and narrower than the right

4. Kidney Renal capsule- fibrous tissue Renal cortex- outer tissue
Medulla-inner tissue with “fans”
Pyramids-12-18/kidney
Papilla-end of the pyramid
Calyx-collects the urine at the end of the papilla
Renal pelvis- calices form it and leads to ureter

5. Renal blood flow Kidneys receive 20-25% of the total cardiac output
Blood flow is ml/min
Renal artery comes off of the abdominal aorta
Exits off the renal vein and into the IVC

6. Nephrons Functioning unit of the kidney Urine is formed from blood
1 million nephrons
Blood comes from the afferent arterioles, enters the glomerulus
Leaves by efferent arterioles

7. Nephron parts Bowman’s capsule surrounds the glomerulus
Proximal convoluted tubule
Loop of Henle
Distal convoluted tubule
Collecting ducts

8. Renin-angiotensin system
Renin is produced by the macula densa cells note changes in the distal convoluted tubules
Based on decreased BP, bld volume and bld NA levels
Renin changes angiotensinogen into angiotensin I, ACE changes it to angiotensin II

9. Angiotensin II Leads to 4 main outcomes:
Increased Na concentration (aldosterone from adrenal cortex)
Increased serum Na level by tubular reabsorption of Na in ascending loop of Henle (constricts afferent arteriole to decrease GFR, if bld volume is low)
Allows fluid to be removed and increases Na concentration in the bld, if blood volume if normal (constricts efferent arteriole to increase GFR)
Enhances reabsorption of Na from DCT

10. Renal regulatory functions
Glomerular filtration- water, electrolytes, Cr, urea N and glucose are filtered
Blood, albuminis too large
Forms 180 L of filtrate/day or GFR=125ml/min
Regulated by constricting and dilating the afferent arteriole
When SBP goes below 70mm Hg, GFR stops (MAP of 60)

11. Tubular reabsorption and Secretion
Most of the water and electrolytes are reabsorbed, 65% of filtrate to keep urine output at 1-3 L
Most of water reabsorption is in the PCT, some is in DCT
DCT is affected by ADH and aldosterone
ADH enhances water reabsorption by increasing membrane permeability
Aldosterone reabsorbs Na
Solute Reabsorption
50% of urea, no creatinine
Most Na, Cl is reabsorbed in the PCT, some in the collecting ducts by aldosterone
K is reabsorbed in the PCT and the ascending loop of Henle
Bicarb, Ca and Phosphate are in the PCT
Glucose is reabsorbed up to 220mg/dl > will be excreted
Tubular secretion is substance need to be excreted, such as K and H

12. Renal hormones Renin= RAAS (renin-angiotensin-aldosterone system)
Prostaglandins- PGE and PGI, regulate filtration and vascular resistance
Bradykinins-dilates the afferent arteriole and increase capillary membrane permeability
Erythropoetin-released when there is decreased oxygen, triggers RBC production in the bone marrow
Vitamin D activation- converted to its active form in the kidney

13. Renal Assessment Personal history- what questions should we ask?
What about diet, why is that important?
What is a normal urine output?
What types of medical conditions can affect the kidneys?

14. Renal Assessment
Inspection- note any swelling or discoloration in the flank region, costovertebral angle is 12th rib and vertebrae
Auscultate for what?
How do you palpate the kidneys?, not be done is suspect pheochromocytoma, what is that?
Percuss what? Only the kidneys or bladder too?

15. Diagnostic tests Urine Blood
Urinalysis for inspection, odor, cloudiness, pH, specific gravity
What is a normal S.G.?
What things would be abnormal in the urine?
How high is the bacterial count in order to be treated?
Blood
Creatinine- end product of muscle and protein metabolism ( )
BUN- excretion of urea N from protein metab, liver failure, trauma will elevate (10-20 mg/dl
Ratio BUN/CR is 12-20:1, dehydration can cause BUN to be elevated, but not CR
Decreased ratio will occur with FVE

16. Diagnostic tests IVP- intravenous pyelogram, now called IV urography
Given a contrast dye, should not give if pt has renal insufficiency
Shows the size, shape and location of kidneys
Patency of calices, pelves and ureters
Detects obstructions and masses

17. Diagnostic Tests
CT of the kidney
Renal Arteriogram

18. Diagnostic Renal Biopsy
Check blood counts before procedure, may need to transfuse
Given procedural sedation
Monitor the site for bleeding 24 hours after, bruising on flank, H&H
Bedrest for 6 hours
Will have hematuria

19. Cystoscopy
Visualize the bladder and any abnormalities

20. Urinary Tract Infections
UTI’s are the most prevalent nosocomial infections, costing 1.6 billion/yr
How can they be prevented in the hospital?
What is the recommended length of time a catheter should remain in, in the acute care setting?
What factors may contribute to a UTI?
Which organisms are most commonly the cause of UTI’s?

21. Urinary Tract Infections
Cystitis- inflammation of the bladder, interstitial cystitis, unknown etiology
Can lead to urosepsis, has a high mortality and prolonged hospitalization
Incidence is greater in women than men and increases by 50% in women over 80

22. Case Study- UTI
24 y.o. sexually active female, who arrives in the ED, complaining of frequency, urgency and dysuria. She has difficulty initiating a stream. This has been occurring for the past 3 days, but not she feels weak and has noticed some blood in her urine

23. Case Study What type of questions may you ask this patient?
What type of urine sample would you get?
The urine comes back with > 100,000 c./ml
Should this be treated? What is the most common antibiotic that is given for an uncomplicated 3 day course?

24. Case Study
What nursing diagnoses would be appropriate for this patient?
What patient education should be done?
Include diet and prevention therapy

25. Urinary Incontinence Incontinence- involuntary loss of urine
Not a normal result of aging
In the elderly, can be caused by:
Medications, disease, depression, unable to walk or get to the BR

26. Types of incontinence
Stress- most common, occurs during coughing, sneezing, jogging or lifting, weakening of the bladder neck can occur with childbirth, can’t tighten the urethra enough to overcome the urge to void
Urge- when they feel the “urge” to go, they can not hold it until they find a BR, called overactive bladder, can be caused by CVA, parkinson’s disease, MS, UTI, BPH, artificial sweeteners, caffeine, alcohol, diruetics, nicotine

27. Incontinence
Overflow- when the detrusor muscle fails to contract, the bladder becomes overdistended, leaks out to prevent rupture, may be urethral obstruction, diabetic neuropathy, pelvic surgery
Reflex- abnormal detrusor contractions r/t neurologic problems- CVA, spinal cord lesions, MS
Functional- loss of cognitive function in patients with dementia

28. Incontinence 85% of all cases are women Contributing factors are:
Medications- diuretics, opioids
Diseases- CVA, arthritis, parkinson’s
Psychological disturbances
Physical examination
Assess for bladder fullness- bladder scan, cystocele, note detrusor muscle

29. Incontinence- Interventions
Exercise- kegel’s strengthen pelvic floor
Weight reduction, decrease fluids at night
Drug therapy- estrogen, antispasmodics- ditropan, probanthine, bentyl, detrol, antidepressants- tricyclics- anticholinergics and alpha-adrenergics, so decrease urination
Vaginal cone- weighted cones to tighten muscles, pessary to hold bladder up in cases of cystocele

30. Incontinence- Surgery
Vaginal or retropubic surgery
Elevates the urethra, repairs cystocele
Postop- monitor voiding, may have SP catheter, PVR should be less than 50ml, monitor for bleeding

31. Incontinence education
What type of education should be provided for bladder training?
How can you get the family to help?
If the patient does need to straight cath or have a foley at home, what things should they monitor for?

32. Renal Calculi- Urolithiasis
Nephrolithiasis- stones in the kidney
Ureterolithiasis- stones in the ureter
75% of the stones contain Ca- Ca oxalate or Ca phosphate
15% struvite, 8% uric acid and 3% cystine
90% of patient have a metabolic risk factor for the stones
Incidence is higher in men

33. Renal calculi Formation is from
Slow urine flow from the element, such as Ca
Damage to the lining of the tract
Decreased inhibitor substances in the urine that would dissolve

34. Renal Calculi Risk Factors
Hypercalcemia-
Increased intake or renal failure
Hyperparathyroidism
Immobilization
Hyperoxaluria-
genetic trait that overproduces
Excess intake from spinach, rhubarb, coca, beets, wheat germ, pecans, okra, chocolate
Hyperuricemia-
Gout with purine metabolism disorder
Increased purines from cancers and thiazide diuretics
Struvite-
Magnesium ammonium phosphate and carbonate, urea splitting bacteria causes
Cystinuria-
Genetic defect of amino acids

35. Renal Calculi Symptoms: Interventions:
Renal colic- what is that?
Oliguria vs anuria, what is the difference?
What is the predominant nursing diagnosis?
Interventions:
Drug therapy:
Pain relief, what should be used?
Besides opioids, what medication may be helpful?
Lithotripsy-
Shock wave therapy to break up stones
Monitor ECG, bleeding after
Strain the urine for stone collection

36. Surgical interventions
Nephrolithotomy and ureterolithotomy
Endoscope or lithotriptor to grasp and extract the stone
Nephrostomy tube is left in place
Keep the nephrostomy site sterile and never irrigate with more than 10 ml
May be performed as an open procedure if the stone is too large

37. Patient education How can the patient prevent getting more stones?
What foods should be avoided if the patient has a calcium oxalate stone? A calcium phosphate stone? A struvite stone? A uric acid stone?
How much fluid should the patient take in per day?

38. Renal Disorders
Polycystic kidney disease- genetic disorder, cysts develop on the kidney, most patients are hypertensive, RAAS is activated
As the patient ages, kidney is more damaged
Controlled by monitoring the BP and using ACE inhibitors, control the cell proliferation of PKD, follow a low NA diet
Control for pain, many need a transplant

39. Polycystic kidney
PKD

40. Glomerulonephritis Third leading cause of ESRD
Disorders that cause are often autoimmune, such as:
Lupus, Goodpasture’s syndrome, Wegener’s granulomatosis, amyloidosis, diabetes, HIV, hepatitis C, cirrhosis, sickle cell disease, endocarditis
Infectious processes also cause, such as:
Beta-hemolytic streptococcus, Staph bacteremia, syphilis, pneumococcal mycoplasma or klebsiella, CMV, histoplasmosis, varicella, toxoplasmosis

41. Glomerulonephritis An infection may precipitate Symptoms occur 10 days
75% of patients have edema of face, hands, eyelids
Fluid overload and circulatory congestion

42. Glomerulonephritis
Urine is smoky or reddish brown with hematuria and oliguria
HTN with wt. gain
Fatigue, anorexia, N&V
What kind of labs would be done?
What lab would be done to assess for a strep infection?
What type of 24 hour urine would be done?

43. Case Study- Nephrotic Syndrome
8 y.o. presents to the hospital with swelling of the face and hands. He has the sickle cell trait. His mother has noted a marked decrease in his urine output and it looks dark brown. He complains of feeling tired and not wanting to eat.

44. Case Study What process occurs with Nephrotic syndrome?
What would you expect to see in his urine? What about his lab values?
His mother asks if this condition can be cured, what would you say?
What type of treatment may be prescribed? Medications and therapy

45. Benign Prostatic Hypertrophy
Prostate become hyperplastic and enlarges with age
Prostate extends upward into the bladder and inward, narrowing the urethral channel
Obstructs urine flow, overflow incontinence
Bladder becomes irritable and leads to urgency and frequency, muscles enlarge and can lead to hydroureters and hydronephrosis

46. BPH Symptoms: Assessment: What nursing diagnoses would be appropriate?
Nocturia
Frequency, urgency
Reduced stream and force
Incomplete emptying and dribbling
Hematuria in elderly males
Assessment:
Digital rectal exam
Urinalysis
PSA level, what is this for?
What nursing diagnoses would be appropriate?

47. BPH
Medications:
Shrink- Proscar, finasteride, lowers DHT, may take 6 months to lower, major side effect is ED and decreased libido
Alpha-adrenergic blockers- Hytrin, Cardura, Flomax, constricts the prostrate and reduces pressure
Avoid medications that may cause urinary retention, such as anticholinergics, antihistamines and decongestants
Don’t take in a large amounts of fluid, avoid alcohol and diuretics, that can cause overdistention

48. BPH Surgery TURP- transurethral resection of the prostate
Can only remove pieces of the prostrate in chip form
Suprapubic, Retropubic and Perineal prostatectomy- done when the prostate is large or the bladder also needs to be explored

49. BPH surgery Postop: Assess incision site if applicable for bleeding
Continuous Bladder irrigation (CBI) done 24 hours post surgery
Monitor for FVE, running total of I & O
Bleeding is to be expected, but urine should not be “frank” blood, may have clots, monitor H&H
May have bladder spasms, ditropan or B&O supp.

50. Renal Failure
Renal failure is the loss of function r/t nephron damage. In CRF, 90-95% of the nephrons are lost before failure is obvious
ARF, only 50% decrease in nephrons can cause failure, ARF is a sudden onset and may last < 3 mo, good prognosis
Most common causes of CRF are:
Diabetes (43%), HTN (25%), glomerulonephritis (8%)

51. Acute Renal failure- ARF
Types of ARF:
Prerenal azotemia- correct by increasing BP, giving volume, improve C.O., prolonged damage can lead to intrarenal failure
Intrarenal- ATN- infections, drugs, NSAID’s, aminoglycosides, tumors, glomerulonephritis

52. Phases of ARF Onset: Oliguric:
Hours to days, precipitating event until oliguria, BUN and Cr increase
Oliguric:
Urine output of ml/day, does not respond to diuretics or fluid challenges, BUN and CR increase, K, Magnesium and Phosphate increase, Na is retained, but masked with fluid, dilutional, lasts 8-15 days

53. Phases of ARF Diuretic: Recovery:
Urine output increases rapidly, can be 10L/day of dilute urine, electrolyte losses occur, BUN decreases last, 2-6 weeks, until BUN falls, renal tubular function returns
Recovery:
Functions at lower level, may take up to 12 months to return to normal
In critically ill patients, 50-80% mortality rate for those who develop ATN

54. Case Study for ARF
25 y.o. male admitted to the ICU post MVA, he had multiple fractures, ruptured spleen and significant blood loss. He has been in the ICU for 24 hours and is ventilated. He has received blood transfusions and maintenance IV fluids, but his blood pressure continues to drop and is presently 80/44, his urine output has only been 100 ml for the past 12 hours.
What do you expect is occurring?

55. Case Study for ARF
What type of ARF is the patient experiencing? What phase is he in?
What can be done to initially correct this problem?
What nursing interventions should be done to monitor for patient improvement?
The MD says that the patient has prerenal azotemia, what does that mean?

56. Case Study- ARF
If the patient is in the oliguric phase, what would the lab values be?
CR –
Bun –
Na –
K –
Phosphorus-
Ca –
Magnesium –
Bicarbonate-
pH-

57. Case Study- ARF
Because of the disruption in electrolytes, what symptoms may the patient experience?
Besides electrolytes, what other labs should the RN monitor? K-
Na-
Phosphate-
Ca- H-

58. Case Study- ARF What are the main Nursing diagnoses for this patient?
What medications may be given to this patient?
Besides replacements, what other meds would be needed?
What should his diet include?
How much protein can he take in?
How much fluid?

59. Case Study- ARF
The patient remains oliguric and has persistent hyperkalemia, FVE and metabolic acidosis, the MD decides that he must begin dialysis to remove the end-products
CRRT is ordered, what does this mean? Why is this done instead of Hemodialysis?
What type of catheter would be inserted? Where is the cath inserted?
Why not have a renal fistula done?

60. Case Study- ARF Prisma machine used for CRRT
Can do hemofiltration, uses a double venous access, one catheter is arterial and one venous return
Changes in fluid removal can be set for every minutes and so they don’t remove as much as regular hemodialysis
Set blood flow at 150ml/hr, dialysate rate at 1L/hr

61. Case Study- ARF
After 5 days on CRRT, the patient’s kidneys begin to improve and his urine output is >30ml/hr, his BP has stabilized and he is off of all vasopressors. He is being transferred to the floor.
What types of things should be still be careful of? What agents may be nephrotoxic to him?

62. Chronic Renal Failure Progressive, irreversible kidney disease
Kidney function does not recover, ESRD
Have azotemia (increased nitrogen wastes), uremia (azotemia with symptoms), uremic syndrome (clinical and labs r/t ESRD)

63. Chronic Renal Failure Stages of CRF:
Stage 1: Diminished Renal Reserve- renal function is reduced, but no accumulation of wastes, can’t concentrate urinepolyuria and nocturia
Stage 2: Renal Insufficiency- wastes accumulate, no response to diuretics, oliguria and edema develop, decreased GFR
Stage 3: ESRD- excessive wastes, BUN and CR, H, treatment is dialysis

64. Chronic Renal Failure Metabolic changes: BUN, CR elevated
Na elevated in later stages, may appear nl or low at first
K elevated, up to 7 or 8 mEq/L, can cause cardiac arrest
H is elevated metabolic acidosis, lungs try to blow off Kussmaul’s respirations
Ca is low, phosphorus is elevated stimulation of PTH, which causes Ca to be released form bone renal osteodystrophy, lack of vitamin D also makes it worse

65. Chronic Renal Failure Cardiac changes: Hematologic: GI changes:
Hypertension- most have because of what?
Hyperlipidemia- changes fat metabolism elevated trigylcerides, cholesterol and LDL
Heart failure- resulting from increased cardiac workload r/t volume, HTN and CAD
Uremic pericarditis- pericardial sac becomes inflammed with toxins pericardial effusion, tamponade and death
Hematologic:
Anemia occurs because of decreased erythropoetin and RBC’s
GI changes:
Ammonia from urea breakdown causes halitosis and stomatitis
Anorexia, N & V occurs, PUD may occur

66. Chronic Renal Failure Clinical Signs: Clinical Signs: Neurologic
Lethargy, seizures, coma from uremia
Cardiovascular
Tachycardia, increased BP, elevated CVP, peripheral edema
Respiratory
Tachypnea, kussmaul’s
Clinical Signs:
Hematologic
Anemia, bleeding, fatigue GI
Abdominal pain, anorexia, foul breath
Urinary
Oliguria, proteinuria, hematuria, amount depends on dialysis
Skin
Yellowish tint, pruitus, uremic frost, purpura and ecchymosis

67. Chronic Renal Failure
What are the common nursing diagnoses for the patient with CRF?

68. Chronic Renal Failure- Interventions
Diet therapy:
Increase calories, but restrict Protein, Fluid, K, Na, Phosphorus, why restrict protein? If the patient is on peritoneal dialysis, protein may be increased
Take vitamins and minerals- return vitamin D, Ca, folic acid

69. Chronic Renal Failure- Interventions
Drug therapy-
Diuretics- only if FVE that is not on dialysis
Biologic response modifiers- procrit
Phosphate binders- amphojel, alternagel, renagel, tums, oscal
Stool softeners- colace, miralax
Vitamins- folic acid, ferrous sulfate
Antihypertensives- ACE, Ca channel and betas may be used

70. Renal Replacement Therapies
Hemodialysis
Better clearance
Short time for treatment
Have to leave home 3x/wk
Can cause disequilibrium syndrome, muscle cramps, hemorrhage
Restricted diet
Peritoneal dialysis
Easy access
Fewer hemodynamic complications
Infections and adhesions can occur
Less effective
Protein loss and peritonitis
Uses intra-abdominal catheter

71. Hemodialysis Used in patients with: Fluid overload Pericarditis
Uncontrolled HTN
Uremic signs
Worsening anemia
Irreversible renal failure when other therapies are not possible

72. Hemodialysis Process:
Diffusion of molecules with the use of dialysate solution, high in electrolytes, water
Waste products move from the blood through the filters semipermeable membrane into the outflow resevoir
Water is also removed by osmosis as it follows the solutes

73. Hemodialysis Hemo filter- over 1 million fine hairs, act as nephrons
Venous access
AV shunt- only short term
Can become dislodged, or bleed

74. Hemodialysis Venous access
AV fistula or graft- artery and vein anastomosed, as it matures, blood flow increases and it enlarges
Do not take BP or blood draws from that arm
Assess pulses
Palpate for thrill and listen for bruits
No lifting of heavy objects

75. Hemodialysis Care
Weigh the patient before and after, know the “dry wt”
Measure BP, HR and Respirations
Watch for orthostatic hypotension
Watch for disequilibrium syndrome- after HD is completed, change in fluid and urea headache, N&V, change in LOC, cerebral edema, seizures, slowing down the fluid removal can prevent it
Bleeding can occur, from heparinization of the lines and low blood counts
Infectious diseases, such as hepatitis C and HIV through blood transmission

76. Peritoneal dialysis
Silastic Catheter is inserted in the abdominal cavity
Dialysate is inserted, dwells for 3-4 hours, allowing fluid to mix with dialysate
Effluent or outflow is then opened and waste products and water are removed

77. Peritoneal dialysis Process is by diffusion and osmosis of products
Dialysate has water and electrolytes, also glucose in 2.5, 5 or 10%, determines the amount of diffusion
Heparin and antibiotics may be added to dialysate
Can be done either throughout the day with a Y-set or at night with an automatic cycler

78. Peritoneal dialysis Tenckhoff, peritoneal catheter Complications
Peritonitis- contamination of catheter, cloudy outflow, fever, abdominal pain and cramping
Pain
Poor outflow and leakage- can be caused by constipation, fibrin clots in the catheter

79. Renal Transplantation
Selection:
Free from medical problems, such as cancer, heart disease and diabetes ( should be under control)
Age is 2-70
Use living and cadaver donors

80. Renal Transplantation
Postoperative Care
Monitor urine output, should return to normal in 48 hours, color may be pink with some clots
Complications:
Rejection
Hyperacute- within 48 hours, fever, pain and increased BP
Acute- 1 wk to 2 yrs, most common, oliguria, fever, enlarged kidney, elevated BUN, Cr
Chronic- months to years, gradual increase in BUN, Cr, fluid retention, fatigue

81. Renal Transplantation
Complications
ATN- may have occurred due to damage to transplanted kidney
Thrombosis- renal artery or vein 2-3 days post
Renal artery stenosis- may lead to hypertension, can often be repaired with a stent
Infections- on immunosuppressives for life
Cyclosporine, prednisone, imuran

82. Renal Transplant Surgery