Renal Problems and
Transplantation
PAUL LOGAN, CRNP
N440
Renal Physiology—BUN
Protein metabolism produces ammonia
◦ Tetracycline, burns, steroids, catabolic state all
produce more NH3
◦ GI bleeding in the PRESENCE of liver disease
makes increased NH3 as blood is digested
◦ (GI bleeding without liver disease just produces
more BUN)
Causes of low BUN
◦ Liver disease; can't make BUN from NH3
Renal Physiology—Creatinine
Laboratory and Diagnostic Tests
BUN
Creatinine
Urine and serum lytes
24 hour urine
Renal ultrasound
Stage
Chronic Kidney
Disease
GFR less than 60 mL/minute for
three months or more,
irrespective of cause
Severity
GFR
(mL/min)
Characteristics
1
Kidney damage with
normal or mild decr.
GFR
≥ 90
Usually none; HTN
2
Mild decr GFR
60-89
Subtle HTN, early bone
disease
3
Mod decr GFR
30-59
Mild HTN, erythropoietin
deficiency, anemia, increased
creatinine
4
Severe decr GFR
15-29
Hyperphosphatemia, met
acidosis, hyperkalemia,
salt/water retention
5
End-stage kidney
disease
< 15
Uremia, severe HTN,
hyperphosphatemia
Causes of CKD
Two most common:
◦ Diabetes (54%) and hypertension (33%)
Other common causes include
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Glomerulonephritis
Interstitial nephritis
Genetic disorders
Hepatorenal syndrome
Microangiopathic
Acute on
Chronic Renal
Failure
It's a thing!
Classification
Acute Kidney
Injury
Affects 5% of hospitalized
patients and has mortality of
50-80%
R-I-F-L-E: Risk-Injury-FailureLoss-End stage
◦ Pre-renal—hypovolemia, hemorrhage, shock, etc.
◦ Intra-renal—acute tubular necrosis (ATN) from ischemia
◦ Post-renal—obstructive
Phases
◦ Oliguria
◦ Anuria
◦ Polyuria
ATN often occurs without anuria, and 10-20% of cases have
no oliguric phase either; this is generally associated with drug
toxicity (e.g. IV contrast), is less severe and generally has a
better clinical course
RIFLE Classification: Grades AKI
Postrenal AKI
About 10% hospital cases
Caused by any obstruction in flow of
urine from collecting ducts in kidneys
to external urethral orifice
Etiologies include
◦ Ureteral obstruction (ie, stones)
◦ Urethral blockage (ie, strictures)
◦ Extrinsic source (ie, tumor)
Diagnostic Tests
• Renal ultrasound—hydronephrosis
Treatments
• Foley catheter
• Suprapubic tube
• Nephrostomy tube
Pathophysiology: Prerenal AKI
Renin–angiotensin–aldosterone cascade
Renal autoregulation
◦ Drugs that interfere with autoregulation include: NSAIDs, ACE inhibitors, ARBs
Changes urinary composition and volume predictable pattern
Etiologies of Intra-Renal AKI
Glomerular
◦ Acute glomerulonephritis
◦ Immune complex–mediated causes
Interstitial—Acute allergic interstitial nephritis
Vascular
◦ Malignant hypertension
◦ Microangiopathic processes
Tubular
◦ Obstructive
◦ Prolonged ischemia
Ischemic ATN
Phases of ATN
Onset phase
◦ Onset hours to days
Oliguric or nonoliguric phase
◦ Lasts 7 to 14 days or 5 to 8 days
(nonoliguric ATN)
Diuretic phase
◦ Lasts 1 to 2 weeks
Recovery phase
◦ Several months to a year
Common Nephrotoxins and ATN
Aminoglycosides
◦ 10% to 20% of patients
◦ Onset delayed, 5 to 10 days after onset
treatment
Contrast-induced nephropathy (CIN)
◦ Occurs within 24 to 48 hours and peaks within 5
to 7 days
◦ High-risk patients
◦ Reduce risk: fluid administration, using low or
iso-osmolar nonionic contrast, N-acetylcysteine
(NAC), alkalinize urine
Comparison of Laboratory Findings
Preventing the Progression
Secondary insults accelerate loss of nephrons.
Include
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Hypovolemia
Nephrotoxic agents
Urinary obstruction and infections
NSAIDs
Hyperglycemia
Hypertension
Hyperlipidemia
Management of Renal Failure
Manage fluid balance changes
◦ Treat hypovolemia
◦ Prevent hypervolemia
Use diuretics
◦ Furosemide, mannitol, thiazide diuretics
Dopamine
Dialysis or ultrafiltration
Manage acid–base alterations
◦ Metabolic acidosis
◦ IV sodium bicarbonate
Manage cardiovascular alterations
◦ Hypertension
◦ Hyperkalemia
◦ Pericarditis
ECG Changes in Hyperkalemia
Management of Renal Failure (cont.)
Managing pulmonary alterations
◦ Pulmonary edema
◦ Pleural effusions, pneumonitis, pulmonary
infections
Managing gastrointestinal alterations
◦ GI bleeding
◦ Anorexia, nausea and vomiting, diarrhea,
GERD
◦ Stomatitis
◦ Constipation
Managing neuromuscular alterations
◦ Sleep disturbances, muscle irritability
◦ Peripheral neuropathies
◦ Seizures
Managing hematological alterations
◦ Increased bleeding tendency
Anemia
Causes include
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Erythropoietin deficiency
Decreased RBC survival time
Blood loss
Other
Management
◦ Administer iron and human erythropoietin.
◦ Blood products
Management of Renal Failure (cont.)
Management of alterations in drug
elimination—Adjust dosages
according to GFR
Management of skeletal alteration
includes loss of bone density and
formation of calcium phosphate
crystals.
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Regulate phosphate.
Maintain calcium levels.
Treat vitamin D deficiency.
Control metabolic acidosis.
Managing of integumentary alterations
include dryness, pruritus, uremic frost,
ecchymosis, and purpura.
◦ Meticulous skin care
◦ Prevent skin breakdown
Managing alterations in dietary intake
◦ Restrict fluid, sodium, potassium, and
phosphate
◦ High calorie, moderate protein restrictions
Managing alterations in psychosocial
functioning
Treatment of Renal Failure
IV fluid
Continuous renal replacement therapy (CRRT)
Diuretic
Hemodialysis
Remove offending agents, like…?
Peritoneal dialysis
Renal dose dopamine
◦ Hits dopamine-1 receptors at low dose, causing
augmented renal blood flow and increased GFR.
◦ Controversial use (is it really dopaminergic, or is
it beta effects?)
Transplantation
General Evaluation
ABO typing
Tissue typing, HLA matching, mixed
lymphocyte culture (MLC) matching
Gastrointestinal evaluation (depending on age
and history)
Gynecological examination
Transfusion history
Electrocardiogram (ECG)
Infectious disease screening
Chest radiograph
Liver function studies
Dental examination to rule out infection
Renal function studies
Social history, review of patient motivation,
ability to follow postoperative regimen, and
psychiatric evaluation
Complete blood count (CBC)
Coagulation studies
Postoperative Phase
VS, oxygenation and ventilator settings, hemodynamics
The patient’s level of consciousness and degree of pain
Number of IV and arterial lines, noting the site, type of solution, and flow rate
Abdominal or chest dressing for drainage, noting the presence of drains and
amount and type of drainage
Presence of bladder and possible ureteral catheters and patency and urinary
drainage
Attachment of nasogastric tube to appropriate drainage system and amount and
character of drainage
Most recent hemodynamic and intraoperative laboratory results
Kidney
Observing the function of the
transplanted kidney
Monitoring fluid and electrolyte
balance
Renal graft function
◦ BUN and creatinine levels
◦ β2-microglobulin level
◦ Renal scan
Helping avoid sources of infection
Urinary drainage problems
Detecting early signs of complications
Urinary leakage—Check dressing,
severe abdominal discomfort or
distention
Supporting the patient and family
through the recovery phase
Patency and the vascular access used
for dialysis
Hyperkalemia—Frequent in acute
postoperative phase
Immunosuppressive Therapy
Suppresses immune response so the transplanted organ is accepted
Provides the recipient with adequate immunosuppression without undue
toxicity, unfavorable reactions, and excess susceptibility to opportunistic
infections
Several drugs may be necessary.
Triple therapy:
◦ Low-dose prednisone
◦ Azathioprine or mycophenolate mofetil
◦ Cyclosporine A or tacrolimus
Complications of Transplantation
Hyperacute rejection
◦ Occurs in OR immediately post-op
◦ Antigen–antibody response
Accelerated rejection
◦ In kidney transplant
◦ Occurs within 1 week; antigen–antibody response
Acute rejection
◦ Occurs within first 3 months
◦ Most common type of rejection; T cells damage.
Chronic rejection
◦ 3 months to years after transplant
◦ Cell-mediated response and response to circulating antibodies
Infection
Most common post-transplant complication
Pre-transplant conditioning and alterations in mucosal barriers conducive to
opportunistic infection
Caused by patient’s own flora
Catheter-associated infections
Wound and lung infections
High risk during first 3 months due to immunosuppressive therapy
Monitor for S & S of infection
Complications
Bleeding
◦ Surgical site, hematoma or lymphocele, result of long-term coagulation therapy, lever
dysfunction, post-op hematuria
Gastrointestinal complications related to steroid therapy
◦ Increased risk of PUD, erosive gastritis
◦ PPI or H2 blockers
Mechanisms of
Graft Rejection
A: Within 24 to 48 hours after
engraftment, dendritic cells that normally
reside within the donor organ migrate to
regional recipient lymphoid tissue. In the
lymph node, they stimulate alloreactive
CD4+ and CD8+ T cells. Activated T cells,
particularly CD4+ cells, produce cytokines
B: There are two types of allorecognition.
Direct allorecognition occurs when T cells
recognize intact foreign major
histocompatibility complex (MHC)
molecules (as depicted in part A). This is
thought to be the dominant initiator of
acute graft rejection. T cells may also
recognize peptide fragments derived
from processing of donor antigens
presented on self-MHC molecules. This is
termed indirect allorecognition, and it is
believed to be important in chronic graft
dysfunction
The End
Renal Physiology