Chronic kidney disease Chronic kidney disease (CKD), also known as chronic renal disease, is a progressive loss of renal

function over a period of months or years. The symptoms of worsening kidney function are unspecific, and might include feeling generally unwell and experiencing a reduced appetite. Often, chronic kidney disease is diagnosed as a result of screening of people known to be at risk of kidney problems, such as those with high blood pressure or diabetes and those with a blood relative with chronic kidney disease. Chronic kidney disease may also be identified when it leads to one of its recognized complications, such as cardiovascular disease, anemia or pericarditis. Chronic kidney disease is identified by a blood test for creatinine. Higher levels of creatinine indicate a falling glomerular filtration rate (rate at which the kidneys filter blood) and as a result a decreased capability of the kidneys to excrete waste products. Creatinine levels may be normal in the early stages of CKD, and the condition is discovered if urinalysis (testing of a urine sample) shows that the kidney is allowing the loss of protein or red blood cells into the urine. To fully investigate the underlying cause of kidney damage, various forms of medical imaging, blood tests and often renal biopsy (removing a small sample of kidney tissue) are employed to find out if there is a reversible cause for the kidney malfunction.Recent professional guidelines classify the severity of chronic kidney disease in five stages, with stage 1 being the mildest and usually causing few symptoms and stage 5 being a severe illness with poor life expectancy if untreated. Stage 5 CKD is also called established chronic kidney disease and is synonymous with the now outdated terms end-stage renal disease (ESRD), chronic kidney failure (CKF) or chronic renal failure (CRF). There is no specific treatment unequivocally shown to slow the worsening of chronic kidney disease. If there is an underlying cause to CKD, such as vasculitis, this may be treated directly with treatments aimed to slow the damage. In more advanced stages, treatments may be required for anemia and bone disease. Severe CKD requires one of the forms of renal replacement therapy; this may be a form of dialysis, but ideally constitutes a kidney transplant. Signs and symptoms Initially it is without specific symptoms and can only be detected as an increase in serum creatinine or protein in the urine. As the kidney function decreases:

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blood pressure is increased due to fluid overload and production of vasoactive hormones, increasing one's risk of developing hypertension and/or suffering from congestive heart failure Urea accumulates, leading to azotemia and ultimately uremia (symptoms ranging from lethargy to pericarditis and encephalopathy). Urea is excreted by sweating and crystallizes on skin ("uremic frost"). Potassium accumulates in the blood (known as hyperkalemia with a range of symptoms including malaise and potentially fatal cardiac arrhythmias) Erythropoietin synthesis is decreased (potentially leading to anemia, which causes fatigue) Fluid volume overload - symptoms may range from mild edema to life-threatening pulmonary edema Hyperphosphatemia - due to reduced phosphate excretion, associated with hypocalcemia (due to vitamin D3 deficiency). The major sign of hypocalcemia being tetany. o Later this progresses to tertiary hyperparathyroidism, with hypercalcaemia, renal osteodystrophy and vascular calcification that further impairs cardiac function. Metabolic acidosis, due to accumulation of sulfates, phosphates, uric acid etc. This may cause altered enzyme activity by excess acid acting on enzymes and also increased excitability of cardiac and neuronal membranes by the promotion of hyperkalemia due to excess acid (acidemia)

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. Diagnosis In many CKD patients, previous renal disease or other underlying diseases are already known. A small number presents with CKD of unknown cause. In these patients, a cause is occasionally identified retrospectively.[citation needed] It is important to differentiate CKD from acute renal failure (ARF) because ARF can be reversible. Abdominal ultrasound is commonly performed, in which the size of the kidneys are measured. Kidneys with CKD are usually smaller (< 9 cm) than normal kidneys with notable exceptions such as in diabetic nephropathy and polycystic kidney disease. Another diagnostic clue that helps differentiate CKD and ARF is a gradual rise in serum creatinine (over several months or years) as opposed to a sudden increase in the serum creatinine (several days to weeks). If these levels are unavailable (because the patient has been well and has had no blood tests) it is occasionally necessary to treat a patient briefly as having ARF until it has been established that the renal impairment is irreversible. Additional tests may include nuclear medicine MAG3 scan to confirm blood flows and establish the differential function between the two kidneys. DMSA scans are also used in renal imaging; with both MAG3 and DMSA being used chelated with the radioactive element Technetium-99. In chronic renal failure treated with standard dialysis, numerous uremic toxins accumulate. These toxins show various cytotoxic activities in the serum, have different molecular weights and some of them are bound to other proteins, primarily to albumin. Such toxic protein bound substances are receiving the attention of scientists who are interested in improving the standard chronic dialysis procedures used today

Stages A Glomerular filtration rate (GFR) <60 mL/min/1.73 m2 for 3 months are classified as having chronic kidney disease, irrespective of the presence or absence of kidney damage. The rationale for including these individuals is that reduction in kidney function to this level or lower represents loss of half or more of the adult level of normal kidney function, which may be associated with a number of complications. All individuals with kidney damage are classified as having chronic kidney disease, irrespective of the level of GFR. The rationale for including individuals with GFR 60 mL/min/1.73 m2 is that GFR may be sustained at normal or increased levels despite substantial kidney damage and that patients with kidney damage are at increased risk of the two major outcomes of chronic kidney disease: loss of kidney function and development of cardiovascular disease. The loss of protein in the urine is regarded as an independent marker for worsening of renal function and cardiovascular disease. Hence, British guidelines append the letter "P" to the stage of chronic kidney disease if there is significant protein loss. Stage 1 CKD Slightly diminished function; Kidney damage with normal or relatively high GFR (>90 mL/min/1.73 m 2). Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies. Stage 2 CKD Mild reduction in GFR (60-89 mL/min/1.73 m2) with kidney damage. Kidney damage is defined as pathologic abnormalities or markers of damage, including abnormalities in blood or urine test or imaging studies. Stage 3 CKD Moderate reduction in GFR (30-59 mL/min/1.73 m 2). British guidelines distinguish between stage 3A (GFR 45-59) and stage 3B (GFR 30-44) for purposes of screening and referral. Stage 4 CKD Severe reduction in GFR (15-29 mL/min/1.73 m2)[1] Preparation for renal replacement therapy Stage 5 CKD Established kidney failure (GFR <15 mL/min/1.73 m2, or permanent renal replacement therapy (RRT)[1] Causes The most common causes of CKD are diabetic nephropathy, hypertension, and glomerulonephritis. Together, these cause approximately 75% of all adult cases. Certain geographic areas have a high incidence of HIV nephropathy. Historically, kidney disease has been classified according to the part of the renal anatomy that is involved, as

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Treatment

Vascular, includes large vessel disease such as bilateral renal artery stenosis and small vessel disease such as ischemic nephropathy, hemolytic-uremic syndrome and vasculitis Glomerular, comprising a diverse group and subclassified into o Primary Glomerular disease such as focal segmental glomerulosclerosis and IgA nephritis o Secondary Glomerular disease such as diabetic nephropathy and lupus nephritis Tubulointerstitial including polycystic kidney disease, drug and toxin-induced chronic tubulointerstitial nephritis and reflux nephropathy Obstructive such as with bilateral kidney stones and diseases of the prostate

The neutrality of this section is disputed. Please see the discussion on the talk page. Please do not remove this message until the dispute is resolved.) The goal of therapy is to slow down or halt the otherwise relentless progression of CKD to stage 5. Control of blood pressure and treatment of the original disease, whenever feasible, are the broad principles of management. Generally, angiotensin converting enzyme inhibitors (ACEIs) or angiotensin II receptor antagonists (ARBs)

are used, as they have been found to slow the progression of CKD to stage 5. Although the use of ACE inhibitors and ARBs represents the current standard of care for patients with CKD, patients progressively lose kidney function while on these medications, as seen in the IDNT and RENAAL studies, which reported a decrease over time in estimated glomerular filtration rate (an accurate measure of CKD progression, as detailed in the K/DOQI guidelines) in patients treated by these conventional methods. Currently, several compounds are in development for CKD. These include, but are not limited to, bardoxolone methyl, olmesartan medoxomil, sulodexide, and avosentan Replacement of erythropoietin and vitamin D3, two hormones processed by the kidney, is usually necessary in patients with CKD, as is calcium. Phosphate binders are used to control the serum phosphate levels, which are usually elevated in chronic kidney disease. When one reaches stage 5 CKD, renal replacement therapy is required, in the form of either dialysis or a transplant. In some cases, dietary modifications have been proven to slow and even reverse further progression. Generally this includes limiting a persons intake of protein Prognosis The prognosis of patients with chronic kidney disease is guarded as epidemiological data has shown that all cause mortality (the overall death rate) increases as kidney function decreases. The leading cause of death in patients with chronic kidney disease is cardiovascular disease, regardless of whether there is progression to stage 5. While renal replacement therapies can maintain patients indefinitely and prolong life, the quality of life is severely affected.[13][14] Renal transplantation increases the survival of patients with stage 5 CKD significantly when compared to other therapeutic options; however, it is associated with an increased short-term mortality (due to complications of the surgery). Transplantation aside, high intensity home hemodialysis appears to be associated with improved survival and a greater quality of life, when compared to the conventional three times a week hemodialysis and peritoneal dialysis.

Why separate acute from chronic renal failure? - Management is different - Manifestations may be similar - Prognosis is different: Chronic Renal Failure – irreversible; Acute Renal Failure – reversible Functions of the Kidney Excretory function Maintenance of Acid – Base Balance Maintenance of Fluid and Electrolyte Balance Maintenance of Ca-Phosphate Balance
(Mineral balance) Measured using: BUN, creatinine pH, HCO3, pCO2 Osmolality, water, Na, K, Cl Ca, Phosphates (Mg)

Vitamin D production Erythropoeitin Production

Calcium Hgb, hct for confirmation

Chronic Renal Failure (CRF) -Pathophysiologic process which is a result of varied conditions that leads to irreversible destruction of nephrons, ultimately leading to End Stage Kidney Disease (ESRD).
-Sum of all processes that happen cause by various diseases such as DM, hpn, GN, lupus, secondary causes due to multiple myeloma, etc. - Slow deterioration of kidney function - Loss of nephrons  other nephrons try to compensate during CRF phase, you don’t see manifestations of ESRD - Normal GFR men:100ml/min; women:85ml/min - Just keep in mind that the key word in CRF is COMPENSATION - DO NOT MAKE THE MISTAKE OF DIALYSING A PATIENT WITH CRF!

Spectrum of CRF: Normal kidney CRF (>3mos) ESRD

Pathophysiology
-Long term reduction of renal mass / function which initially leads to compensatory hypertrophy and function. Eventually this leads to sclerosis of the remaining nephron, resulting to ESRD.

Stages of Chronic Renal Disease Stage 1 Description At increased risk of kidney damage with normal or increased GFR Kidney damage with mildly decreased GFR Moderately decreased GFR Severely decreased GFR Renal Failure (ESRD) GFR, mL/min per 1.73 m2 90 (with CRD risk factors) 90 60-89 30-59 15-29 < 15

2 3 4 5

GFR
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CRF: 16-89 mL/min ESRD: <15 mL/min

Difference between CRF & ESRD in terms of Pathophysiology CRF – there is hyperfiltration, some amount of compensation ESRD – no more compensation; all other organ systems will end up with some kind of dysfunction Kidney Function Excretory Function Chronic Renal Failure (CRF) No signs / symptoms ↑ BUN ↑ Creatinine, ↑ Cystatin C No Manifestations End-Stage Renal Disease (ESRD) Nausea / vomiting ↑↑ BUN ↑↑ Creatinine, ↑↑ Cystatin C ↑ RR – Kussmaul

Maintenance of Acid-

Base Balance Maintenance of Fluid & Electrolyte Balance

Normal acidbase balance

↑ BP NVE Crackles Edema Na – Normal K – Normal or ↑ Maintenance No of Calcium- manifestations Phosphate ↑ Phosphate Balance ↓ Ca Vitamin D No Production manifestations ↓ Calcitriol (see diagram below) Erythropoiet Weakness in Dizziness Production Pallor Easy Fatigability ↓ Hemoglobin

breathing Metabolic Acidosis ↑ RR Arrythmia NVE Crackles Edema Na – Normal K–↑ Osteitis fibrosa cystica ↑↑ Phosphate ↓↓ Ca Osteomalacia ↓ Calcitriol

Weakness Dizziness Pallor Easy Fatigability ↓↓ Hemoglobin

Excretory function: • ≤1.5mg creatinine • 10-20 BUN depending on level of hydration • Cystatin- only used in lab research for now Maintenance of Acid-Base Balance: • Still with compensation Maintenance of Fluid & Electrolyte Balance: • For fluids, think also of sodium going along with it • Creatinine clearance >60, accumulation of Na • Increased BP: CM, lupus, GN • No signs/symptoms, normal BP: may also have renal failure, creatinine worsening • Buko juice: causes hyperkalemia; so AVOID DRINKING BUKO JUICE WHEN YOU HAVE KIDNEY PROBLEMS UNLESS YOU HAVE LOW POTASSIUM • Buko juice, bananas  good fore people with diarrhea • Nephrologists should therefore identify patients are Na or K wasters. If this is the case then don’t let them avoid Na of K. Maintenance of Calcium-Phosphate Balance • >25% creatinine clearance is still normal Vitamin D Production • Calcitriol- only in lab research for now • (Please refer to table at last page) Why is there an increase in phosphates in ESRD?  because the poorly functioning kidney can’t eliminate them all. The phosphate binds with calcium  leading to a decrease in ionized calcium  leading to secondary hypoparathyroidism Erythropoietin Production • In DM, anemia occurs early

Management of Chronic Renal Failure

A. Comprehensive strategy for renoprotection in patients with chronic renal disease Intervention Therapeutic Goal Specific renoprotective therapy Proteinuria <0.5 g/day ACE inhibitor or GFR decline <2 ARB treatment ml/min/year Specific renoprotective therapy Proteinuria <0.5 g/day ACE inhibitor or GFR decline <2 ARB treatment ml/min/year Adjunctive cardiorenal protective therapy Additional <130/80 mm Hg antihypertensive therapy Dietary protein restriction 0.6-0.8 g/kg/day Dietary salt 3-5 g/day restriction Tight glycemic AIC < 6.05 % control in diabetes Normal values Reduce elevated calcium-phosporous Lipid lowering therapy Anti-platelet therapy Consider correction of anemia Smoking cessation Weight control
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LDC-C <100mg/dl Thrombosis prophylaxis Hb > 12g/dl Abstinence Ideal body weight

Level of proteinuria determines the level of dietary protein restriction in patients Reduce elevated electolyte Ca and P if <25%, it merits checking The lecturer considers correction of anemia if Hb 11-12g/dl Lipid lowering therapy (Statins)

B. Avoid insults to the kidney •Volume depletion- diarrhea •Nephrotoxins- aminoglycosides, radiocontrast material •NSAID- COX2 inhibitors, mefenamic acid, naproxene, indomethacin C. Preparation for ESRD management • Psychological • Renal Replacement Therapy, options o Dialysis – Vascular Access

o Transplant – Recipient Donor Work-Up * with a creatinine clearance of 20 or 25, you can start discussing dialysis with the patient

End Stage Renal Disease
Please see table on first page Excretory function:  Nausea and vomiting- SSX of accumulation of BUN, creatinine Maintenance of Acid-Base Balance: • metabolic acidosis Maintenance of Fluid & Electrolyte Balance: • body can’t eliminate waste products because it can’t compensate; arrhythmia due to increased K Maintenance of Calcium-Phosphate Balance • Phosphate retained, binds to Ca, absence of Vit D3 decreased gut absorption of Ca Vitamin D Production Erythropoietin Production

•Anemia insidious in onset  so you may have SSX in ESRD
Pathophysiology: fibrosis – no more compensation in whatever aspect of excretion

Management of ESRD
A. Supportive 1. Nutrition 2. Psychological 3. Control BP 4. Maintain Hb at 110-120 g/dl with erythropoietin oral iron is not absorbed very\well by uremic patient; it’s better to give it to
them IV

5. Fluid and electrolyte balance 6. Acid-base homesotasis 7. Maintain Ca and Phosphate balance – B. Renal Replacement Therapy 1. Dialysis 2. Hemodialysis 3. Peritoneal Dialysis 4. Transplant 5.

give Calcium carbonate or Calcium acetate with meals. You eat meat, and meat has phosphate. Para habang nakakapagbigay ka ng calcium, nakakapag prevent ka na rin ng absorption ng phosphate. You “shoot two birds with one stone”

- Consider dialysis if creatinine clearance is about 20ml/min - Uremic symptoms present with nausea and vomiting. If the disease is not ESRD, consider other etiologies for the said symptoms - Excess fluid in the body – volume overload – diuretics won’t help coz kidneys are already sclerosed

Renal Replacement Therapy in CRF - indicated when metabolic abnormalities can no longer be controlled with conservative management or when signs and symptoms of uremia developed - No absolute value in terms of CR by which you will start your RRT Indications for Dialysis - volume overload

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intractable metabolic acidosis hyperkalemia uremic state (encephalopathy, pericarditis) azotemia without uremic manifestations

CASE A 24-year old male diagnosed with chronic glomerulonephritis was admitted for nausea and vomiting. Maintenance of ACE inhibitors with HCTZ (Hydrochlorothiazide) was given. His last follow-up a week ago showed a Cr 1.8 mg%. Three days PTA he had copious diarrhea and was unable to take anything including medicines. He noted decreased urine output. He felt weak and later developed nausea and vomiting. PE: BP = 90/60 PR = 110/min RR = 25/min Sunken eyeballs, dry skin and mucous membranes BUN 80mg/dL; Cr 10mg/dL; K 6meq/L; Na 132 meq/L ABG: pH 7.2; HCO3 11meq/L; CO2 20meq/L Hgb: 15gm/dl (N14-17) Hematocrit: 45 (hemoconcentrated) Urinalysis: Sp gr = 1.010, (4+) protein, (–) sugar 4-5 RBCs/hpf, 10-15 WBCs/hpf What is your diagnosis? a. Acute renal failure b. Chronic renal failure c. End stage renal failure d. Acute on chronic renal failure Answer: Acute on Chronic Renal Failure What finding tells us that the patient has renal failure? a. K b. pH c. creatinine d. urinalysis –just a reflection that something’s wrong, but not specific for renal failure Answer: Creatinine What is the cause of the ABG finding? e. Chronic GN f. Diarrhea g. Vomiting h. Acute renal failure Answer: Diarrhea and ARF (acidosis)

How should you manage this patient? a. kidney transplant b. dialysis c. supportive management d. observe Answer: Supportive Management
Management:  Hydrate patient


  

For increased K, give sodium bicarbonate- shoot two birds with one stone  not only do you decrease K you also replace the lost HCO3 Treat the cause of diarrhea Nutrition: don’t focus on it yet. Just follow treatment for diarrhea Follow up BUN, creatinine. If it improves, don’t do anything. Take note that there’s a 3-4 day period before creatinine drops.

Hypovolemia: low BP, sunken eyeballs, dry skin, mucous membrane Increased RR implies metabolic acidosis Hemoconcentration due to diarrhea

If the creatinine changed from 1.8 to 9mg, but the patient has nausea and vomiting, Bp=130/80, no diarrhea, eyeballs not sunken, (+)edema, what is the management?
Decreased Renal Function

Answer: Dialysis
AI3+ Intoxication Accumulation of ß2 microglobulin

Hyperphosphatemia

Decreased 1.25 (OH)2D3

If anemic (Hb 10g/dl), what is the mgt? Answer: Give erythropoietin. If <10 g/dl, transfusion
From block B:  Hyperkalemia – don’t give diuretics because patient is dehydrated; give sodium bicarbonate -> push K inside the

Decreased expression of calciumsensing receptor

Decreased ionized Ca2+

Hyperparathyroidism

Hyperplasia of the parathyroid glands

Osteitis fribrosa cystica (high-turnover bone disease)

Osteomalacia

Adynamic bone disease

Dialysis-related amyloidosis

Metabolic acidosis

Excess Ca and vit D, PD, diabetes

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