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Chronic Kidney Disease (CKD) Is a disease whereby the kidneys have trouble removing waste products and fluid

from the body. Usual causes of CKD include Diabetes Mellitus, high blood pressure and chronic glomerulonephritis. People with CKD often have no symptoms although the kidney function is severely affected. With chronic kidney disease (CKD), the kidneys don't usually fail all at once. Instead, kidney disease often progresses slowly over a period of years. This is good news because if CKD is caught early, medicines and lifestyle changes can possibly help delay disease progression.

Stages of CKD The stages of CKD (Chronic Kidney Disease) are mainly based on measured or estimated GFR (Glomerular Filtration Rate). There are five stages but kidney function is normal in Stage 1, and minimally reduced in Stage 2. Stage 1 2 3A 3B 4 GFR* 90+ 60-89 45-59 30-44 15-29 Description Treatment stage Normal kidney function but urine findings or structural abnormalities or genetic Observation, control of blood pressure. trait point to kidney disease Mildly reduced kidney function, and other findings (as for stage 1) point to Observation, control of blood pressure and risk factors. kidney disease Moderately reduced kidney function Observation, control of blood pressure and risk factors. Planning for endstage renal failure. Medication and a special diet or renal replacement by dialysis or renal transplant.

Severely reduced kidney function Very severe, or endstage kidney failure (sometimes called established renal 5 <15 or on dialysis failure) 2 * All GFR values are normalized to an average surface area (size) of 1.73m Suffixes:

p suffix: the addition of p to a stage (e.g. 3Ap, 4p) means that there is significant proteinuria T - the addition of T to a stage (e.g. 3AT) indicates that the patient has a renal transplant. D - the addition of D to stage 5 CKD (e.g. 5D) indicates that the patient is on dialysis

Definition of chronic: Labelling someone as having CKD requires two samples at least 90 days apart. Historical values can be used.

Signs and Symptoms People with chronic kidney disease suffer from accelerated atherosclerosis and are more likely to develop cardiovascular disease than the general population. Patients afflicted with chronic kidney disease and cardiovascular disease tend to have significantly worse prognoses than those suffering only from the latter. A person with Stage 5 CKD has end stage renal disease (ESRD) with a GFR of 15 ml/min or less. At Stage 5 kidney disease, your kidneys are no longer able to remove waste and fluids from the body effectively which leads to a build-up of toxins in the blood. Most people at Stage 5 CKD will need dialysis or a kidney transplant. Patient in this stage of CKD may experience symptoms such as:

Loss of appetite Nausea and/or vomiting Headaches Fatigue

Trouble concentrating Itching Little or no urine Swelling, especially around the eyes and ankles

Muscle cramps Tingling in hands or feet Changes in skin color Increased skin pigmentation

Stage 5 CKD is very severely reduced kidney function (endstage or ESRF/ESRD), less than 15% (eGFR less than 15 ml/min). Creatinine and eGFR in an individual are usually quite stable. Deteriorating renal function needs rapid assessment. Note that CKD staging and management outlined below are only applicable to stable renal function. Assessment and management of stable Stages 4 and 5 CKD. Initial assessment is identical to Stage 3 CKD, but in contrast to Stage 3, referral to or discussion with a specialist service will be usual. Exceptions to 'always refer or discuss' may include patients in whom: severe renal impairment is part of another terminal illness those in whom all appropriate investigations have been performed and there is an agreed and understood care pathway those in whom further investigation and management is clearly inappropriate. Initial assessment of stages 4 and 5 CKD Is the patient well? Is there a history of significant associated disease? If assessment is precipitated by a first discovery of elevated creatinine, it is important to be certain that the value is stable. Maybe there are previously recorded values? If not, and the patient is well, repeat test within 14 days. Ideally this sample should be taken after a period of at least 12h without meat consumption, and the sample must get to the lab or be separated the same day. Deteriorating renal function needs rapid assessment. Clinical assessment - especially for sepsis, heart failure, hypovolaemia, examination for bladder enlargement (imaging indicated if obstruction suspected from symptoms or examination), cardiovascular system. Medication review - any potentially nephrotoxic drugs, or drugs that need dose alterations when GFR reduced?

Urine tests: dipstick for blood and quantitation of proteinuria by ACR/PCR. Presence of haematuria or proteinuria may suggest progressive renal disease. Blood tests: Ca, PO4, Hgb. Imaging - exclusion of obstruction is indicated in patients with singnificant urinary symptoms or other things to suggest obstruction. As above, referral or discussion is usual.

Management of stable Stages 4 and 5 CKD Typically 3 monthly estimation of Creatinine and K - hyperkalaemia that is severe or not responsive to changes in therapy should lead to discussion or referral. Hgb - if low, exclude non-renal cause. Ca and phosphate - Oral phosphate binders will often be necessary. Urinary protein for ACR or PCR. Note thresholds; ACR 30 or PCR 50 for more stringent blood pressure targets (and suffix 'p' on CKD stage), and ACR 70 or PCR 100 for specialist referral/discussion. More on proteinuria Blood pressure - 140/90 max (130-139/90), or 130/80 max (120-129/80) for patients with proteinuria: urinary ACR>30 or PCR>50. More on hypertension Cardiovascular risk - advice on smoking, exercise and lifestyle. Consider cholesterol lowering therapy if already have macrovascular disease, or if estimated 10 year risk of cardiovascular events =/>20%. Immunization - influenza and pneumococcal, plus hepatitis B immunization if renal replacement therapy contemplated. Medication review - regular review of medication to minimise nephrotoxic drugs (particularly NSAIDs) and ensure doses of others are appropriate to renal function. o In osteoporosis/ low bone density, do not use bisphosphonates or other agents that reduce bone turnover without detailed assessment of possibility of renal osteodystrophy. Specialist discussion required.

There are two types of dialysis: hemodialysis and peritoneal dialysis Hemodialysis requires that an access be created to get the blood from your body to the dialyzer (artificial kidney) so it can be cleaned and then go back into your body. Because in stage 5 the kidneys are no longer working, dialysis must begin soon. A catheter will be placed into a vein in the neck, chest or groin. This is considered a temporary access. If you decide to remain on hemodialysis, your nephrologist will likely recommend you get a fistulacreated, which is a permanent access. To create a fistula, an artery and vein are surgically connected in the forearm. It takes a few months for the fistula to mature so that it can be used for dialysis. There is another type of access called a graft that uses artificial tubing to connect the artery and vein. It takes three to six weeks to heal so that it can be used for dialysis. For PD, a catheter access is placed in the abdomen. PD is performed by running dialysate solution through the catheter into the peritoneum and then removing the solution after a time and replacing it with new dialysate. The peritoneal membrane that lines the peritoneum is a semipermeable membrane that does the filtering for the kidney. There are different methods of performing PD. Some people manually drain and fill their abdomen every four to six hours, which is called continuous ambulatory peritoneal dialysis (CAPD). Others use an automated machine, called a cycler, which works while they sleep and then do a manual exchange in the morning. This is called

continuous cycler peritoneal dialysis (CCPD). There is another choice called nocturnal intermittent peritoneal dialysis (NIPD) where PD is performed at night while sleeping. With NIPD, no exchanges are done during the day. Most people report feeling much better once they begin dialysis. As the toxins are removed from their blood and they receive medicines that replace the functions the kidneys can no longer perform, they find they can enjoy a good quality of life. Changes in the diet Once you begin dialysis, you will need to make changes in what you eat and drink. Your diet is a big part of your treatment, so you will be working with a dietitian who will coach you on how you should eat. Depending on the dialysis treatment you choose and your lab test results, your dietitian will help create a meal plan based on your individual requirements to keep you feeling your best. People on hemodialysis generally need to increase their protein, and limit fluids, sodium, potassium and phosphorus, and in some cases, calcium. Those who choose PD usually need to increase their protein and limit phosphorus, but may have fewer limits on fluid and potassium. Your dietitian will explain what foods are restricted and which ones are recommended on the renal diet. A healthy diet for stage 5 CKD may recommend:

Including grains, fruits and vegetables, but limiting or avoiding whole grains and certain fruits and vegetables that are high in phosphorus or potassium A diet that is low in saturated fat and cholesterol and moderate in total fats, especially if cholesterol is high or if you have diabetes or heart disease Limiting intake of refined and processed foods high in sodium and prepare foods with less salt or high sodium ingredients Aiming for a healthy weight by consuming adequate calories and including physical activity each day within your ability Increasing protein intake to the level determined by the dietitians assessment of individual needs and to replace losses in the dialysis treatment Taking special renal vitamins high in water soluble B vitamins and limited to 100 mg of vitamin C Vitamin D and iron tailored to individual requirements Limiting phosphorus to1000 mg or based on individual requirements Limiting calcium to 2000 mg (no more than 1500 mg from calcium based phosphorus binders). Limiting potassium to 2000 to 3000 mg or bases on individual requirements

Anemia of CKD Kidneys have an important role in keeping your blood healthy. People with chronic kidney disease may develop anemia. Anemia becomes an increasing problem in CKD as GFR falls. Severe renal anemia is uncommon before at least stage 3B, 4 and 5 CKD. You should be offered a blood test to see if you have anemia. Other causes need to be considered, but when not present, Erythropoietin-like drugs (epoetins) and intravenous iron management is the mainstay of management and greatly improved patient symptoms and quality of life. If you are anemic and have chronic kidney disease, it does not necessarily mean that your anemia is caused by the kidney disease there are many other possible causes of anemia. Investigation and management of anemia in CKD

Exclude other causes of anemia When Hgb falls far below 10-11g/dl, treatment with intravenous iron erythropoiesis stimulating agents may be considered Treatment aims to maintain Hgb between 11 and 12 g/dl. Lower levels of Hgb are acceptable if the Hgb fails to rise despite adequate iron replacement and epoetin therapy.

There are likely to be local algorithms and protocols for management of renal anemia. These may include different treatment initiation and target Hgb values Calcium, phosphate and bones Calcium and phosphate metabolism are upset in moderate to severe CKD, and marked disturbances in either should usually lead to referral for detailed assessment, or enquiries for advice. Severe disturbances are usually restricted to stages 4 and 5 CKD. The aim in Stage 3+ CKD is to keep [Ca] normal, serum phosphate at or below 1.8 mmol/l, and PTH below twice (to three times) the upper limit of normal. Calcium is commonly low-normal or low in renal failure. High PTH is a physiological response to low calcium and to the phosphate retention that occurs in renal failure. Often dietary advice and phosphate binders taken with food are needed to keep phosphate within acceptable limits. Vitamin D derivatives (alfacalcidol, calcitriol) are used to correct hypocalcaemia resulting from reduced renal activation of vitamin D, and also have a direct suppressive effect on PTH secretion. Initiation of these agents is usually a matter for specialist advice. High calcium causes renal impairment. If it is a presenting feature in a patient with kidney disease, the hypercalcemia or the cause of hypercalcemia must be suspected to be the cause of the renal problem. In treated CKD it may be caused by oral calcium and vitamin D treatment, or by tertiary hyperparathyroidism.

Cardiovascular risk Patients with CKD have greatly increased risks of cardiovascular events and cardiovascular deaths. Furthermore, when events occur, their morbidity and mortality is higher. This increased risk begins when there is microalbuminuria even with normal GFR, or when GFR falls below about 50. It is known that the Framingham tables significantly underestimate the risk of cardiovascular disease in patients with CKD. These observations reinforce the importance of controlling cardiovascular risk factors. Recommendations: General

Smoking cessation Weight loss

Aerobic exercise Limiting salt intake

Chronic Glomerulonephritis Chronic glomerulonephritis is the advanced stage of a group of kidney disorders, resulting in inflammation and slowly worsening destruction of internal kidney structures called glomeruli. It occurs when there is slow, progressive destruction of the glomeruli of the kidney, with progressive loss of kidney function. In some cases, the cause is found to be a specific attack to the body's immune system, but in most cases, the cause is unknown. Damage to the glomeruli affects the kidney's ability to filter fluids and wastes properly. This leads to blood and protein in the urine. This condition may develop after survival of the acute phase of rapidly progressive glomerulonephritis. In about one-quarter of people with chronic glomerulonephritis there is no prior history of kidney disease, and the disorder first appears as chronic kidney failure. Causes include:

Diabetic nephropathy/sclerosis Focal segmental glomerulosclerosis IgA nephropathy (Berger's disease) Lupus nephritis

Membranous glomerulonephritis Mesangial proliferative disorder Nephritis associated with disorders such as amyloidosis, multiple myeloma, or immune disorders, including AIDS

This condition causes high blood pressure (hypertension) and chronic kidney failure. Specific symptoms include:

Blood in the urine (dark, rust-colored, or brown urine)

Foamy urine

Chronic kidney failure symptoms that gradually develop may include the following:

Decreased alertness
o o o

Generalized itching Headache Increased skin pigmentation -- skin may appear yellow or brown Muscle cramps Muscle twitching Nausea and vomiting Need to urinate at night Seizures Unintentional weight loss

Drowsiness, somnolence, lethargy Confusion, delirium Coma

Decreased sensation in the hands, feet, or other areas Decreased urine output Easy bruising or bleeding Fatigue Frequent hiccups General ill feeling (malaise)

Additional symptoms that may be associated with this disease:


Blood in the vomit or stools Excessive urination

High blood pressure Nosebleed

BULACAN STATE UNIVERSITY MALOLOS CITY, BULACAN COLLEGE OF NURSING

Submitted by: Maria Fatima C. Bagay BSN III-A

Submitted to: Sir Marlon Robles, RN

Pathophysiology (Based on the patients case) Non-Modifiable Factors: -Hereditary/Congenital -Age -Gender -Race Diabetic nephropathy / sclerosis Focal segmental glomerulosclerosis IgA nephropathy (Berger's disease) Modifiable Factors -Diet -Lifestyle -Environment

Lupus nephritis

Membranous glomerulonephritis

Mesangial proliferative disorder

Acute Glumerulo Nephritis leading to Chronic Glumerulo Nephritis Repeated inflammation Stage 1 GFR (>90mL/min/1.73m2) Ischemia Nephron loss Decrease renal blood flow Increased BUN Increased Serum Creatinine Damage to nephrons Stage 2 GFR (60-89mL/min/1.73m2) Stage 3 GFR (30-59mL/min/1.73m2) Renal insufficiency Remaining nephrons undergo changes Remaining nephrons filter more solutes Stage 4 GFR (15-29mL/min/1.73m2) Dilute Polyuria Hypertrophy of remaining nephrons Inability to concentrate urine Further loss of nephron functions Stage 5 GFR <15mL/min/1.73m2) Loss of non-excretory renal function Failure to produce erythopoietin Anemia Loss of Sodium in Urine Hyponatremia Dehydration Shrinkage of kidney

Decrease renal reserve

Decrease glomerular filtration

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