1 Renal Problems and TransplantationPaul logan, CRNP N440

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4 Renal Physiology—BUN Protein metabolism produces ammoniaTetracycline, 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

5 Renal Physiology—Creatinine

6 Laboratory and Diagnostic TestsBUN Creatinine Urine and serum lytes 24 hour urine Renal ultrasound

7 Chronic Kidney DiseaseStage 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 GFR less than 60 mL/minute for three months or more, irrespective of cause

8 Causes of CKD Two most common: Other common causes includeDiabetes (54%) and hypertension (33%) Other common causes include Glomerulonephritis Interstitial nephritis Genetic disorders Hepatorenal syndrome Microangiopathic

9 Acute on Chronic Renal FailureIt's a thing!

10 Acute Kidney Injury Classification PhasesPre-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 Affects 5% of hospitalized patients and has mortality of % R-I-F-L-E: Risk-Injury-Failure- Loss-End stage

11 RIFLE Classification: Grades AKI

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13 Postrenal AKI About 10% hospital casesCaused 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

14 Pathophysiology: Prerenal AKIRenin–angiotensin–aldosterone cascade Renal autoregulation Drugs that interfere with autoregulation include: NSAIDs, ACE inhibitors, ARBs Changes urinary composition and volume predictable pattern

15 Etiologies of Intra-Renal AKIGlomerular Acute glomerulonephritis Immune complex–mediated causes Interstitial—Acute allergic interstitial nephritis Vascular Malignant hypertension Microangiopathic processes Tubular Obstructive Prolonged ischemia

16 Ischemic ATN Phases of ATN Onset phase Oliguric or nonoliguric phaseOnset 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

17 Common Nephrotoxins and ATNAminoglycosides 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

18 Comparison of Laboratory Findings

19 Preventing the ProgressionSecondary insults accelerate loss of nephrons. Include Hypovolemia Nephrotoxic agents Urinary obstruction and infections NSAIDs Hyperglycemia Hypertension Hyperlipidemia

20 Management of Renal FailureManage 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

21 ECG Changes in Hyperkalemia

22 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

23 Anemia Causes include Management Erythropoietin deficiencyDecreased RBC survival time Blood loss Other Management Administer iron and human erythropoietin. Blood products

24 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. 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

25 Treatment of Renal FailureIV fluid Diuretic Remove offending agents, like…? 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?) Continuous renal replacement therapy (CRRT) Hemodialysis Peritoneal dialysis

26 Transplantation

27 General Evaluation ABO typingTissue typing, HLA matching, mixed lymphocyte culture (MLC) matching Transfusion history Infectious disease screening Liver function studies Renal function studies Complete blood count (CBC) Coagulation studies Gastrointestinal evaluation (depending on age and history) Gynecological examination Electrocardiogram (ECG) Chest radiograph Dental examination to rule out infection Social history, review of patient motivation, ability to follow postoperative regimen, and psychiatric evaluation

28 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

29 Kidney Observing the function of the transplanted kidneyMonitoring fluid and electrolyte balance Helping avoid sources of infection Detecting early signs of complications Supporting the patient and family through the recovery phase Patency and the vascular access used for dialysis Renal graft function BUN and creatinine levels β2-microglobulin level Renal scan Urinary drainage problems Urinary leakage—Check dressing, severe abdominal discomfort or distention Hyperkalemia—Frequent in acute postoperative phase

30 Immunosuppressive TherapySuppresses 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

31 Complications of TransplantationHyperacute 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

32 Infection Most common post-transplant complicationPre-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

33 Complications BleedingSurgical 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

34 Mechanisms of Graft RejectionA: 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

35 The End

36 Renal Physiology