RENAL DISORDERS power point presentation

Renal disorders

1. RENAL DISORDERS Dr. J. Mutinda

2. Acute Pyelonephritis Pyelonephritis is a bacterial infection of the renal pelvis, tubules, and interstitial tissue of one or both kidneys. Bacteria reach the bladder by means of the urethra and ascend to the kidney. Pyelonephritis is frequently secondary to ureterovesical reflux. Urinary tract obstruction, bladder tumors, strictures, benign prostatic hyperplasia, and urinary stones are some of the other causes.

3. Clinical manifestations The clinical manifestations of acute pyelonephritis vary from mild fatigue to the sudden onset of chills; fever; vomiting; malaise; flank pain. Others are lower urinary tract manifestations: cystitis, dysuria, urgency, and frequency. Costovertebral tenderness to percussion, bacteriuria and pyuria usually persist.

4. Assessment and diagnostic findings Urinalysis results indicate pyuria , bacteriuria , and varying degrees of hematuria. A complete blood count shows leukocytosis Urine culture and sensitivity tests are performed An ultrasound study or a CT scan may be performed to locate any obstruction in the urinary tract

5. Medical management Pregnant women and Patients with severe infections or complicating factors such as nausea and vomiting with dehydration require hospitalization. Others are treated as out patients. Parenteral antibiotics are often given initially in the hospital

6. When acute symptoms resolve and the patient is stable he/she is discharged on oral antibiotics. Adequate fluid intake Antipyretic and analgesic drugs to reverse fever and relieve pain and discomfort

7. Nursing interventions Nursing interventions vary depending on the severity of symptoms. They include teaching the patient about the disease process with emphasis on: (1) continuing medications as prescribed, (2) having a follow-up urine culture, and (3) recognizing manifestations of recurrence or relapse

8. Glomerulonephritis Glomerulonephritis is the inflammation of the glomeruli. A variety of conditions can cause glomerulonephritis, ranging from kidney infections to systemic diseases. Glomerulonephritis can be acute or chronic

9. Causes/ risk factors for glomerulonephritis Throat infection- Post streptococcal glomerulonephritis may develop 1-2 wk after a streptococcal throat infection. Antibodies cause inflammation Viral infections- Viral infections can trigger GN. Common viruses include the HIV and hepatitis B & C viruses. Systemic lupus erythematosus - Autoimmune disorder characterized by the involvement of several tissues and organs, particularly joints, skin, and kidneys

10. Acute Glomerulonephritis Glomerulonephritis is an inflammation of the glomerular capillaries. Pathophysiology - Most cases of acute glomerulonephritis develop 5 to 21 days after an infection of the tonsils, pharynx, or skin or by nephrotoxic strains of group A β-hemolytic streptococci. The inflammation process results in antigen-antibody complexes being deposited in the glomeruli

11. Clinical manifestations At times the patient may be asymptomatic- diagnosed on routine urinalysis. The clinical manifestations include: Generalized body edema & oliguria – due to decreased glomerular filtration Hypertension- results from increased extracellular fluid volume Hematuria with a smoky appearance- Smoky urine indicates bleeding in the upper urinary tract

12. Proteinuria- The degree varies with the severity of the glomerulonephropathy . The patient may have abdominal or flank pain. Elderly patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema. Atypical symptoms include confusion, somnolence, and seizures, which are often confused with the symptoms of a primary neurologic disorder.

13. Assessment and diagnosis The diagnosis is based on a complete history and physical examination. Assessment of antistreptolysin -O (ASO) titers. A renal biopsy may be done to confirm the Dx Urinalysis and urine sediment microscopy reveal erythrocytes in significant numbers. Proteinuria may range from mild to severe. Blood tests:-BUN and serum creatinine to assess the extent of renal impairment.

14. Multidisciplinary management The management of acute glomerulonephritis focuses on symptomatic relief. Rest is recommended until the signs of glomerular inflammation (proteinuria, hematuria) and hypertension subside. Edema is treated by restricting sodium and fluid intake and by administrating diuretics.

15. Severe hypertension is treated with antihypertensive drugs. Dietary protein intake may be restricted if there is elevated BUN & proteinuria. If streptococci are found in the culture, treatment with appropriate antibiotic therapy is essential

16. Nursing care- Acute phase The nurse observes the patient for changes in fluid and electrolyte status and for signs and symptoms of deterioration of renal function. Changes in fluid and electrolyte status and in cardiac and neurologic status are reported promptly to the physician. Provides emotional support by allowing the patient and family to verbalize their concerns, have their questions answered, and explore their options. Administer Rx

17. Home based Nursing care Teaching Patients Self-Care- Fluid and diet restrictions must be reviewed with the patient to avoid worsening of edema and hypertension. The patient is instructed to notify the physician if symptoms of renal failure occur (e.g. fatigue, nausea, vomiting, diminishing urine output) or at the first sign of any infection.

18. Follow up care- Stress the importance of follow-up evaluations of blood pressure, urinalysis for protein, and serum BUN and creatinine levels to determine if the disease has progressed.

19. Preventive measures To prevent the disorder encourage early diagnosis and treatment of sore throats and skin lesions. Encourage the patient to take the full course of antibiotics. Good personal hygiene is an important factor in preventing the spread of cutaneous streptococcal infections.

20. NEPHROTIC SYNDROME Nephrotic syndrome is a primary glomerular disease characterized by: proteinuria, edema, hypoalbuminemia and hyperlipidemia. Pathophysiology - It results when the glomerulus is excessively permeable to plasma protein, causing proteinuria that leads to low plasma albumin and tissue edema. Efforts by the liver to increase the production of albumin fail, thus, hypoalbuminemia results

21. Causes Causes include chronic glomerulonephritis, diabetes mellitus with intercapillary glomerulosclerosis, systemic lupus erythematosus, multiple myeloma, and renal vein thrombosis. Nephrotic syndrome can occur with almost any intrinsic renal disease or systemic disease that affects the glomerulus

22. Clinical manifestations Nephrotic syndrome is characterized by the loss of plasma protein, particularly albumin, in the urine. Pitting oedema most commonly occurring around the eyes, in dependent areas (sacrum, ankles, and hands), and in the abdomen (ascites). hypercoagulability results from the urinary loss of anticoagulant proteins

23. Immune responses are altered in nephrotic syndrome leading to infections. Other symptoms, including malaise, headache, irritability, and fatigue, are common

24. Diagnostic tests Characteristic laboratory findings include decreased serum albumin, decreased total serum protein, and elevated serum cholesterol. The urine may also contain increased WBCs as well as granular and epithelial casts. A needle biopsy of the kidney may be performed for histologic examination of renal tissue to confirm the diagnosis.

25. Collaborative management Cyclophosphamide and prednisone may be used for the treatment of nephrotic syndrome. Use of medications to control Diabetes. Some individuals may need thiazide or loop diuretics, anticoagulants, immunosuppressants. The treatment of hyperlipidemia includes lipid-lowering agents, such as colestipol.

26. Increased protein intake with emphasis on high biologic proteins. Dietary salt restrictions are a key to managing edema.

27. Nursing care Instruct patients on importance of following all medication and dietary regimens so that their condition can remain stable as long as possible. Assess the edema by weighing the patient daily, accurately recording fluid intake and output, and measuring abdominal girth or extremity size. Clean the edematous skin carefully. Avoid trauma to the skin.

28. Monitor the effectiveness of diuretic therapy. Anorexia- Serve small, frequent meals in a pleasant setting to encourage better dietary intake Infection prevention- teach the patient to avoid exposure to persons with known infections. Support the patient to cope with an altered body image.

29. ACUTE KIDNEY INJURY AKI/ARF is a clinical syndrome characterized by rapid loss of renal function with progressive azotemia (increase of nitrogenous wastes such as BUN and creatinine). Electrolyte and fluid status changes with few symptoms: Uremia- Accumulation of urea in the blood renal function declines to a point that symptoms develop in multiple body organs.

30. Oliguria - reduced urine output to below 400ml/day. Patients with nonoliguric ARF recover faster with few complications while those with oliguric ARF have a poor outcome. ARF develops within hrs or days with progressive increase in BUN, creatinine and K+ with or without oligura .

31. Causes

32. Prerenal causes Any condition that decreases blood flow, blood pressure, or kidney perfusion before arterial blood reaches the renal artery that supplies the kidney. Causes include: Prolonged hypotension (sepsis, vasodilation ) Prolonged low cardiac output (heart failure, cardiogenic shock) Prolonged volume depletion (dehydration, hemorrhage) Renovascular thrombosis ( thromboemboli )

33. Intrarenal causes Any condition that produces an ischemic or toxic insult directly at parenchymal nephron tissue places the patient at risk for development of intrarenal AKI. Acute tubular necrosis (ATN) is the most common intrarenal cause of AKI and is primarily the result of:

34. Kidney ischemia, blood transfusion reactions, muscle injury etc Endogenous toxins (tumor lysis syndrome) Exogenous toxins ( radiocontrast dye, nephrotoxic medications) Infection (acute glomerulonephritis , interstitial nephritis)

35. Postrenal causes Any obstruction that hinders the flow of urine from beyond the kidney through the remainder of the urinary tract may lead to postrenal AKI May occur due to obstruction (urethra, prostate, or bladder)

36. Clinical course of AKI Initiating phase- From insult till features become apparent. Lasts hrs to days. Oliguric phase- It occurs 1- 7 days following kidney injury and lasts 10-14 days If the cause is ischemia oliguria occurs within 24 h The longer it is the poorer the outcome Urine output less than 400ml/24hrs, casts, RBCs, WBC in urine, high SG and urine osmolality Fluid volume excess: oedema, bounding pulse.

37. Metabolic acidosis; decreased HCO3- Na normal or reduced k+ excess (worsened by acidosis)- ECG changes Hematologic disorders- leucocytosis Ca2+ deficit and phosphate excess Waste product accumulation- BUN & creatinine Neurologic disorders- accumulation of waste

38. Diuretic phase- Gradual increase in daily urine output of 1-3l/24 hrs due to osmotic diuresis from high urea conc in the glomerular filtrate and inability of tubules to concentrate urine. Can lead to hypotension and electrolyte imbalance. Lasts 1-3 wks and electrolyte levels, BUN, creatinine , acid-base start to normalize.

39. Recovery phase-glomerular Filtration rate increases leading to reduced BUN and creatinine. Although major improvements occur in the first 1 to 2 weeks of this phase, it take upto 12 months to stabilize or may progress to Chronic renal failure.

40. Clinical manifestations Urinary – reduced output, protenuria , casts, reduced SG, reduced U osmolality, increased urinary Na+ (Hypo natremia may lead to cerebral oedema). CVS- volume overload, hypertension ; HF, pericarditis, pericardial effusion, dysrhythmias. Respiratory system- pulmonary oedema, kussmaul respiration, pleural effusion

41. GIT- N&V, anorexia, stomatitis, bleeding, diarrhea, constipation. Hematologic- anemia, increased susceptibility to infections, leukocytosis, defective platelet function Neurologic- lethargy, seizures, memory impairment. Metabolic- increased BUN, creatinine, Na+, k+, PH, HCO3-, decreased Ca2+, Po

42. Disease states that predispose one to AKI

43. Heart failure There is a strong association between kidney failure and heart failure. Several of the risk factors for atherosclerotic cardiovascular disease are also detrimental to the kidney over the long term, notably hypertension and diabetes.

44. Respiratory Failure and Acute Kidney Injury There is a significant association between respiratory failure and kidney failure. Acute hypoxic respiratory failure and can predispose patients to develop acute kidney injury (AKI) Mechanical ventilation can alter kidney function- Positive-pressure ventilation reduces blood flow to the kidney, lowers the GFR, and decreases urine output.

45. Sepsis and Acute Kidney Injury Sepsis and septic shock create hemodynamic instability and reduce perfusion to the kidney. Immunologic, toxic, and inflammatory factors may alter the function of the kidney microvasculature and tubular cells.

46. Catheter-Associated Urinary Tract Infection Critically ill patients who have a protracted illness have a significant risk of contracting a CAUTI, especially if the catheter is required for several days The key components of CAUTI prevention include: 1. Avoid unnecessary use of urinary catheters 2. Insert urinary catheters using aseptic technique 3. Review the need for the urinary catheter daily and remove promptly

47. MANAGEMENT

48. Fluid replacement The objectives of volume replacement are to replace fluid and electrolyte losses and to prevent ongoing loss. Maintenance IV fluid therapy is initiated when oral fluid intake is inadvisable. Treatment of prerenal causes of AKI

49. Fluid Restriction Fluid restriction is used to prevent circulatory overload and the development of interstitial edema when the kidneys cannot remove excess volume. Patients with kidney failure are usually restricted to 1 L of fluid per 24 hours if the urine output is 500 mL or less

50. Fluid Removal Acute kidney failure results in retention of fluids, solutes and toxins Conservative therapy may be all that is necessary until kidney function improves. Renal replacement therapy

51. Pharmacologic management Use of diuretics- Diuretics reduce volume overload and are helpful for symptoms such as pulmonary edema, but they have not been shown to prevent AKI.

52. Nutrition The recommended energy intake is between 20 and 30 kilocalories/kg per day, with 1.2 to 1.5 grams/kg of protein per day to control azotemia (increased BUN level). Oral nutrition is preferred, and if the patient cannot eat, enteral nutrition is recommended over parenteral nutrition.

53. Potassium and sodium are regulated in accordance with plasma levels. Sodium is restricted as needed to prevent edema, hypertension, and HF.

54. Nursing care Acute phase

55. Prevention of Infectious Aseptic technique is critical. Protect the patient from other individuals with infectious diseases. Be alert for local manifestations of infection (e.g., swelling, redness, pain), as well as systemic manifestations (e.g., fever, malaise, leukocytosis). Administer the prescribed antibiotics

56. Management of Fluid and electrolyte balance Monitoring for I and O (to include fluids removed with dialysis) Monitoring for signs of overhydration. Take daily weights Monitor electrolyte levels- Hyperkalemia, hypocalcemia, hyponatremia, hyperphosphatemia, and acid–base imbalances occur during AKI

57. Clinical manifestations of these electrolyte imbalances must be prevented and their associated side effects controlled. The more likely imbalances are hyperkalemia and hypocalcemia, which can result in life-threatening cardiac dysrhythmias. Dilutional hyponatremia may develop as fluid overload worsens in the patient with oliguria

58. Other care interventions Perform skin care and take measures to prevent pressure ulcers because the patient usually develops edema and decreased muscle tone. Mouth care is important to prevent stomatitis, which develops when ammonia in saliva irritates the mucous membranes.

59. Health promotion To prevent renal failure: Careful monitoring of intake and output and fluid and electrolyte balance is essential. Assess and record extrarenal losses of fluid from vomiting, diarrhea, hemorrhage, and increased insensible losses. Prompt replacement of significant fluid losses helps prevent ischemic tubular damage associated with trauma, burns, and extensive surgery.

60. Monitoring Weight- an indicator of volume status Nephrotoxic drugs should be used sparingly in the high-risk patient. Caution the patient about abuse of over-the-counter drugs

61. Chronic kidney disease Progressive irreversible loss of kidney function. Presence of kidney damage or GFR less than 60ml/min for 3 months or longer -(Normal GFR is 125ml/min). Kidney damage- pathologic abnormalities or markers of damage with abnormalities in blood or urine tests or imaging studies.

62. Causes The leading causes are diabetes (about 50%) and hypertension (about 25%). Less common etiologies include glomerulonephritis, cystic kidney diseases, and urologic diseases .

63. Stages of chronic renal disease Stage 1- Kidney damage with normal or decreased GFR GFR ≥ 90ml/min/1.73m 2 ; GRF= 90% and above. Intervention- Diagnose and treat comorbid conditions, CVD risk reduction Stage 2- Kidney damage with mild reduction in GFR GFR is 60-89ml/min/1.73m 2 =60- 89% GFR. Intervention- Estimate progression

64. Stage 3 Moderate reduction in GFR- GFR is 30-59 ml/min/1.73m2 i.e. 30-59% GFR Intervention- Evaluate and treat complications Stage 4 Severe reduction in GFR i.e. 15-29% GFR GFR is 15-29ml/min/1.73m 2 Rx- Prepare for renal replacement therapy

65. Stage 5=ESRD Kidney failure GFR ˂1ml/min/1.73m 2 or dialysis <15% Rx- Renal replacement if uremia present

66. Clinical manifestations of Chronic Renal disease Occur due to retained substances i.e. urea, creatinine, hormones, electrolytes, water etc Uremia- syndrome that incorporates the features seen in various body systems in a pt with CKD. Neurologic problems- fatigue, headache, sleep disturbances, lethargy, muscle irritability, seizures, confusion, coma

67. Psychologic - denial, anxiety, depression, psychosis. CVS- HTN, HF, atherosclerotic heart disease, pericarditis , cardiomyopathy , pericardial effusion GIT- anorexia, N &V, uremic fetor (urinous odor of breath), GIT bleeding, PUD, gastritis, stomatitis

68. Endocrine / reproductive- thyroid abnormalities, amennorhea , infertility, sexual dysfunction, azoospermia Metabolic- CHO intolerance, hyperlipidemia, nutritional defects, gout. Hematologic- anemia, bleeding, infection Occular - hypertensive retinopathy

69. Pulmonary- uremic lung, pulmonary edema, uremic pleuritis , dyspnea , pneumonia and depressed cough reflex. Peripheral neuropathy- parasthesias , motor weaknesses, restless legs syndrome Musculoskeletal- Muscle cramps; loss of muscle strength; bone pain; bone fractures; foot drop.

70. Diagnostic tests Dipstick evaluation of proteinuria, albuminuria, Albumin to creatinine ratio- A ratio greater than 300 mg albumin per 1 g creatinine signals CKD. Urinalysis test for RBC,WBC, glucose, casts. Serum creatinine values and estimate GFR in order to stage CKD; Urine culture Imaging of kidneys- US to detect any obstructions and to determine the size of the kidneys Hematocrit and HB levels

71. Collaborative therapy Correction of extracellular fluid volume overload through renal replacement therapy. Nutritional therapy Ca++ supplements, phosphate binders or both Antihypertensive therapy, inslulin for hyperkalemia Alluminium - based antacids bind dietary phosphates in the GIT. Antiseizure drugs, Erythropoietin. Adjustment of drug doses to degree of renal function.

72. Renal trauma Renal trauma can be blunt or penetrating. Renal trauma is especially likely when the patient injures the abdomen, flank, or back especially in sports injuries, motor vehicle collisions, and falls. Penetrating injuries may result from violent encounters The severity of renal trauma depends on the extent of the injury

73. Clinical manifestations Clinical findings include a history of trauma to the area of the kidneys. Gross or microscopic hematuria may be present.

74. Diagnosis & Treatment Diagnostic studies include urinalysis, ultrasound, CT, or MRI, Renal arteriography. Both the injured kidney and the uninvolved kidney should be evaluated. Treatments range from bed rest, fluids, and analgesia to exploratory surgery and repair or nephrectomy.

75. Nursing interventions Assess the cardiovascular status and monitor for shock, especially in a penetrating injury ensure adequate fluid intake and monitor intake and output; provide for pain relief and comfort measures; and assess for hematuria