1. Chapter 26 Acute Kidney Injury and Chronic Kidney Disease

2. Acute Kidney Injury (AKI)
A rapid decline in kidney function sufficient to increase blood levels of nitrogenous waste and impair fluid and electrolyte balance
Potentially reversible if underlying cause is corrected or removed
Mortality rate 40-90%
Seen more often in older adults, usually superimposed on other life-threatening conditions
Most common indicator is azotemia and GFR

3. Types of Acute Kidney Injury
Prerenal
Postrenal
Intrarenal (Intrinsic)

4. Prerenal AKI Most common form of AKI
Characterized by a marked decrease in renal blood flow
Reversible if the cause of blood flow can be identified before kidney damage occurs
Causes
Profound depletion of vascular volume (hemorrhage, loss of ECF)
Impaired perfusion (CHF, cardiogenic shock, vasoactive mediators-drugs/diagnostic agents)
Decreased vascular filling (anaphylaxis, sepsis)

5. Prerenal AKI Manifested by a sharp decrease in urine output
Disproportionate elevation in BUN in relation to serum creatinine (ratio greater than 15:1)

6. Vasoactive Mediators Stimulate intense intrarenal vasoconstriction
Can induce glomerular hypotension and prerenal failure
Drugs
Endotoxins
Radiocontrast agents
Cyclosporine
NSAIDs

7. Impaired Renal Adaptive Mechanisms
ACE inhibitors and ARBs reduce the effects of renin on blood flow
Can convert compensated renal hypoperfusion into prerenal failure
When combined with diuretics, may cause prerenal failure in persons with decreased renal blood flow (large/small vessel disease)
NSAIDs can reduce renal blood flow

8. Renal Blood Flow
Kidneys normally receive 20 to 25% of the cardiac output
Normal kidney can tolerate relatively large reductions in blood flow before renal damage occurs
As renal blood flow  , GFR  , amount of Na+ and other substances 
When blood flow falls 20-25% below normal ischemic changes
Tubular epithelial cells are most vulnerable to ischemic injury and can lead to ATN (acute tubular necrosis)

9. Acute Tubular Necrosis
Tubular epithelial cells have a high metabolic rate
Most vulnerable to ischemic injury

10. Postrenal AKI
Results from obstruction of the ureter, bladder or urethra
Obstructs outflow of urine from the kidneys
Retrograde pressure occurs throughout the tubules and nephrons damages the nephrons
Both ureters of functioning kidneys must be obstructed to cause AKI
Treatment is aimed at treating the underlying cause

11. Intrarenal AKI
Results from conditions which cause damage to structures in the kidney
Damage to the parenchyma in the glomeruli, vessels, tubules or interstitium
Most common cause is injury to the tubules
Precipitating factors:
Ischemia associated with prerenal failure
Toxic insult to the tubular structures of the nephron
Intratubular obstruction
Acute glomerulonephritis
Acute pyelonephritis

12. Acute Tubular Necrosis (ATN) and Injury
Characterized by the destruction of the tubular epithelial cells with acute suppression of renal function
Ischemic
Extensive surgery, severe hypovolemia, overwhelming sepsis, trauma or burns
Nephrotoxic
Aminoglycosides, chemotherapy

13. Phases of ATN Onset (Initiating Phase)
The time from onset of the precipitating event until tubular injury occurs
Maintenance
Oliguric or non-oliguric (non-oliguric has better outcome)
Characterized by a marked in GFR
Sudden retention of endogenous metabolites
Fluid retention edema, water intoxication and pulmonary congestion
Hypertension, signs of uremia
Neuromuscular irritability seizures coma death

14. Phases of ATN Recovery Repair of renal tissue takes place
Gradual increase in urine output
Fall in serum creatinine (nephrons are recovering)
Diuresis
Renal function restored

15. Nursing Implications Attention should be focused on prevention
Identification of persons at risk
Preexisting renal insufficiency
Diabetics
Elderly
At risk persons taking
Nephrotoxic drugs (IV contrast, aminoglycosides)
NSAIDs

16. Nursing Implications Careful observation of urine output
Earlier assessment of AKI
Urine tests for osmolarity, urinary sodium concentration, fractional excretion of sodium can differentiate from prerenal azotemia
Urinalysis (proteinuria, hemoglobinuria, myoglobinuria, casts or crystals)
GFR- best real-time indicator of current kidney function
New diagnostic biomarkers
Neutrophil gelatinase-associated lipocalin (NGAL)
Cystatin C
Tissue inhibitor mettaloproteinase-2 (TIMP-2)

17. Nursing Implications Early identification and correction of cause
Maintain normal fluid volume and electrolyte concentrations
Adequate caloric intake
Prevention and treatment of infections
Hemodialysis of CRRT (continuous renal replacement therapy)

18. Question
Which type of acute kidney injury (AKI) would be most likely to accompany benign prostatic hypertrophy?
Prerenal
Postrenal
Intrinsic
Intrarenal

19. Answer
B. Postrenal
Rationale: Postrenal AKI occurs when the flow of urine is blocked by kidney stones, tumors, or an enlarged prostate gland. Because the male urethra passes through the prostate, if it is enlarged, the urethra may become blocked.

20. Chronic Kidney Disease
Pathophysiologic process that results in the loss of nephrons and a decline in renal function as determined by a GFR for > 3 months
Caused by DM, HTN, SLE, glomerulonephritis, PCKD
Prevalence and incidence is growing
Onset is insidious
Remaining nephrons undergo structural and functional hypertrophy

21. Chronic Kidney Disease (cont.)

22. Diagnosis of CKD GFR Normal is 120 to 130 ml/min
GFR < 60 represents a loss of ½ or more of the level of normal function
Proteinuria
Urinary albumin preferred in adults and adolescents
Microalbuminuria (early sign of CKD in diabetics)

23. Chronic Kidney Disease

24. Manifestations of CKD Fluid, electrolyte, acid-base disorders
Cardiovascular complications
Gastrointestinal disorders (nausea, anorexia)
Disorders of mineral metabolism
Hematologic complications
Immunological disorders
Neuromuscular complications
Sexual dysfunction (impotence, impaired sexual function))
Skin disorders (pruritis, dry skin, subcutaneous bruising)

25. Fluid, Electrolyte and Acid-Base Disorders
Sodium and water balance
Dehydration or fluid overload
Inability to concentrate urine and regulate sodium
Potassium balance
Compensatory mechanism until renal function is severely compromised hyerkalemia
Acid base balance
Hydrogen ion secretion, sodium and bicarbonate reabsorption is impaired metabolic acidosis (stabilizes as the disease progresses)

26. Cardiovascular Complications of CKD
Major cause of death in persons with CKD
Hypertension – early manifestation (vascular volume, peripheral vascular resistance, activity of RAAS
Treated with salt and water restriction and antihypertensive drugs
Heart disease
LVH
Ischemic heart disease
CHF

27. Mineral Metabolism Disorders in CKD
Calcium, phosphorus, PTH and Vitamin D
Hyperphosphatemia, hypocalcemia, active vitamin D levels, hyperparathyroidism
Metastatic calcifications
In arteries, visceral organs and joints
Bone disease – renal osteodystrophy
Reductions in bone mass
Bone pain
Skeletal fracture

28. Neuromuscular Complications of CKD
Peripheral neuropathy
Restless leg syndrome
Uremic encephalopathy
Dosorders of motor function
Reduction in alertness and awareness

29. Hematologic Complications of CKD
Anemia: from hemolysis, bone marrow suppression, decreased erythropoietin and iron
Weakness, fatigue, depression, insomnia, decreased cognitive function
Decreased blood viscosity  increased heart rate, peripheral vasodilation
Angina pectoris and other ischemia
Decreased platelets  bleeding

30. Stages of CKD

31. Treatment of CKD-Conservative
Conservative management to prevent or slow down the rate of nephron destruction
BP and blood glucose control
ACE inhibitors or ARBs
Smoking cessation
Dietary management
Restriction of proteins, sodium, phosphorus and fluid

32. Medication Management
CKD interferes with absorption, distribution and elimination of drugs
Many drugs are bound to plasma proteins with the unbound portion free to act at receptor sites and metabolized
Decreased plasma protein results in greater amounts of free drug
Drugs and toxic metabolites can accumulate
Dosing needs to be adjusted
Caution patients to avoid OTC drugs

33. Treatment of CKD-Renal Replacement Therapy
Hemodialysis
Artificial kidney
3-4 times per week
S/E = hypotension, n/v, muscle cramps, H/A, chest pain
Peritoneal dialysis
Thin serous membrane of the peritoneal cavity serves as the dialyzing membrane
Transplantation

34. Hemodialysis System

35. Peritoneal Dialysis

36. CKD in Children
Caused by congenital malformations, inherited or acquired disorders, metabolic syndromes
Manifestations: growth impairment, developmental delay, delay in sexual maturation, bone abnormalities and psychosocial problems
Treated with CCPD or NIPD
Early transplantation is best approach