INTRODUCTION
Renal Impairment is one of the leading public health issue across the globe, ultimately which is urge for emergency care, morbidity, mortality rate and reduce in quality of life, an augment in serum creatinine concentrations greater than 0.5 to 0.90 mg/dL has been associated with a 6-5 fold increase in the odds of death, 1,2In a chronic stage which also exacerbate for other health issues like cardiovascular disorders3,4and increase in economic cost of life5It is noted to be the 12th leading cause of death with approximately 85000 deaths in a year6, As well decline in glomerular functioning observed in chronic stages and in old age people. Kidneys are primarily involved in excretion of drug, Where as decrease in glomerular function rate (GFR) leads to accumulation of drug metabolites in the body which causes of accumulation in body of toxic materials which again worse the condition. In addition, the plasma protein binding of drugs may be extensively decreased, which in turn could persuade the ADME8. Hence, a dosage adjustment is possible to be needed for rationale use in such a population where the renal function is impaired and the drug or its active metabolites exhibit a narrow therapeutic index and when excretion and / or metabolism occurs primarily via renal organs.
In a heath care setting safety of the patient is a prime and main concern across the globe. Most of the individuals are victim of medication errors which can be reduced approximately up to 25%-11.Few research articles conclude that incidence of adverse drug reaction(ADR,s) high when compared to other patients. In addition it’s observed that incidence of Drug Related Problems (DRP’s) are high among the patients those who are suffering with chronic kidney diseases12. Poor outcome for errors may be mild to severe. For instance, patients with severe renal insufficiency receiving allopurinol are more prominent which can be life threatening toxicity syndrome accompanied by erythematous, skin rash, hepatitis, pyrrexia, eosinophilia and deterioration of kidney function is common in people those who receive first line therapy at a dose of 200-400mg in a day. In screening of 72 patients 8 found to be fatal who received allopurinol13. Excretion rate of metformin is extended in renal failure which causes increase lactic acidosis carriers a in a patients those also represents any of the one disease among the following. Kidney Impairment, myocardium failure, chronic hepatic disorders, large doses and age > 80 years14. Maximum of the antimicrobials which build up toxic metabolites in patients those who are represented with renal failures. Neuromuscular toxicity, myoclonus seizures, or coma can be observed with high serum levels with the use of injectables like penicillin G or carbenicillin15, Toxic metabolites of nitrofurantoin may accumulate in patients with renal failure, which ultimately leads to peripheral neuritis16. 10.6% of deaths are reported in Nepal those patients who live their life in countryside, on other hand another study reported similar ratio in developed places.17 Where as in India a large difference is observed in the people according to their living places.18
It is needed to be tampering of the dose either reduction in the maintenance dose and/or an increase in the dose interval for the drugs which have narrow therapeutic index, or parent drugs or active metabolite which are firstly eliminated by renal organs have to managed to minimize potential adverse drug events (ADE) and improve the therapeutic outcome. By applying Clinical pharmacy services which prevents potential DRP’s.19
Renal failure or renal insufficiency is a medical situation characterized by decline in renal function which is unable to filter metabolic wastes from the blood and body.
CLASSIFICATION OF KIDNEY FAILURE
What is Acute Renal Injury?
Acute renal injury (AKI) or Acute renal failure (ARF) is characterized is a prior stage to CKD where a rapid fall in renal function consequently leads inappropriate fluid maintenance, disturbed body electrolyte and acid-base balance and homoeostasis.20 ARF also characterized by increased creatinine, urea, and other metabolic waste products (azotemia).21
Classification of Acute Kidney Injury / Acute Renal Failure
Stage Serum Creatinine GFR Rate Urine Output
1
Risk S. Cr increases of ≥0.3 mg/dLSCr of ≥1.5-2.0-fold Decrease by 25% <0.5 mL/kg/h for 6 h
2
Injury S. Cr increases of ≥2.0–3.0-fold Decrease by 50% <0.5 mL/kg/h for 12 h 3 Failure S. Cr increase of ≥0.3 mg/dL or >3-fold from baseline
S. Cr ≥4.0 mg/dL with acute increase ≥0.5 mg/dL Decrease by 75%
Decrease by >75% <0.3 mL/kg/h for 24 h
Anuria for 12 h
Who is at risk of developing acute kidney injury?
The occurrence of acute renal failure (ARF) and chronic renal failure (CRF) is more common in the people those who are aged above 64 years, 22 Other comobrbidties like diabetes mellitus, hypertension, obesity and proteinuria are self-governing risk factors for ARF.23, 24 When it is mixed irrational use of medicines, including nephrotoxic medicines are likelihood of an acute- or chronic decline in renal function.
Types and Causes of Acute Renal Failure:
Pre-Renal Failure: Decrease in a blood flow to renal organs is the most commonest cause of AKI, Which is because of failure in auto regulation in maintenance of renal flow.25Consistent decrease in kidney perfusion heightens the inherent kidney failure (acute tubular necrosis), which leads to permanent damage to renal organs.
The main causes of pre-renal injury are:
Hypovolaemia, e.g. In a severe condition of diarrhoea, vomiting, diuretics, osmotic diuresis from poorly glyceamic control, hemorrhage and traumatic or septic shock
Decreased effective blood volume, e.g. heart failure or cirrhosis
Vasoregulation, e.g. Drugs like analgesics and other NSAIDs, Chemotherapeutic agents, Anti tubercular agents, angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs), or hypercalcaemia.25
Post-renal injury: It is due to interruption in the normal micturation, resulting in a back pressure to renal organs leads to nephron damage. This obstructive nephropathy and is a relatively exceptional cause of acute kidney injury (5%). Timely diagnosis and treatment can lead to a complete recovery.
The most frequent causes of obstructive nephropathy include:
Urinary tract stones
Prostatic hypertrophy
An intra-abdominal process encasing the ureters, e.g. retroperitoneal fibrosis or prostatic and other pelvic malignancy.25
Intrinsic renal injury: It results due the injury of renal tubules, glomerulus, vascular structures, or obstruction of the renal tubules21 which is the most commonest cause of nephron damage and acute tubular necrosis is the leading among them, Which results in toxicity (hypotension, hypovolaemia, haemolysis, rhabdomyolysis or nephrotoxic medicines, e.g. NSAIDs, lithium or aminoglycosides).25,26 Approximately 90 % of Acute Renal failure is because of history with pre-renal injury and acute tubular necrosis.
Drugs which can cause interstitial nephritis or intrinsic acute renal injury :
Furosemide,
Proton Pump Inhibitors,
Beta-Lactam Antibiotics,
Aminoglycosides,
Cyclosporin,
Sulphonamides,
Colchicine,
Phenytoin,
Lithium and Paracetamol (High Dose or Chronic Use).26,27
CLINICAL MANIFESTATION
The characteristics of ARF starts from the various conflicts of renal functioning that are associated with the disease. Clinical presentations includes such as fatigue, loss of appetite, headache, nausea and vomiting due to the accumulation of urea and nitrogenous substance in blood stream.28
Increased level of potassium causes arrhythmia, which can fatal29
Haemostatic mechanism will be disturbed which causes elevated blood pressure either it can be high, low or normal.30
Inflammation to renal organ causes the pain in the flank region of the body.31
CHRONIC KIDNEY DISEASE
The National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) explains that CRF is the presence of renal damage or a decreased functioning rate of glomerular.(GFR<60ml/min/1.73m2) for duration of 90 days or longerwith or without kidney damage.32 The glomerular filtration rate (GFR), which is most commonly estimated (eGFR) using equations that include serum creatinine concentration along with demographic data, is the most frequently used index of overall kidney function.33,34 This condition is frequently not associated with significant symptoms until the disease is far advanced or urinary abnormalities and is unrecognized in 80–90% of cases.35 CKD are at high risk for progress to ESRD, a condition requiring renal replacement therapy, i.e., dialysis or kidney transplantation, to keep the patient’s long-term survival.33,34 The definition of stages 1 and 2 CKD is based upon manifestations of renal damage, i.e., the presence of either micro- or macro-albuminuria, erythrocyturia, or abnormalities on renal ultrasound. Determination of the eGFR in these earlier stages is required only to differentiate between stages 1 and 2 (eGFR >90 or between 60–89 mL min−1 per 1.73 m−2 , respectively). These early stages of CKD are mostly asymptomatic i.e. the normal of kidney functions, but the possibility for advanced disease is significant. As kidney disease worsens, kidney function begins to deteriorate (stages 3 and 4 CKD). Eventually, kidney failure (stage 5 CKD) arises, and kidney replacement therapy is required. Stages 3, 4, and 5 are exclusively defined by GFR (eGFR 30–59, 15–29 or <15 ml min-1 per 1.73 m-2 respectively.)35 The K/DOQI chronic kidney disease staging system (Table 1) is based on GFR.32 Stages of CKD with their GFR values Risk factors for early chronic kidney disease: The following risk factors are associated with a significant (20–40%) risk of CRF: Obesity Hypertension Diabetes mellitus Cigarette smoking Established CVD Age > 60 years
Familial history of stage 5 CKD or hereditary kidney disease in a first or second degree relative
Severe socioeconomic disadvantage.
Presences of renal calculi (6% absolute risk)
Alcohol abuse and Benign prostatic hypertrophy.36
Most common complications and comorbidities of CRF include
Fluid and Electrolyte Abnormalities,
Anaemia,
Secondary Hyperparathyroidism and Renal Osteodystrophy,
Hypertension and hyperlipidaemia, metabolic acidosis, and several other comorbidities involving malnutrition, pruritus and uremic bleeding.37
The most common symptoms of CKD are
Fatigue or Lack of Energy
Nausea, Vomiting
Metallic Taste in Mouth/ Amonia Breath
Feeling Drowsy,
Muscle Cramps and Flank Region Pain
Shortness of Breath
Swelling of Hands and Feet’s
Puffy Face and Pruritus etc.38
DIFFERENT CAUSES OF EFFECTING KIDNEY DISEASE
There are certain other causes which leads to ARF or CRF of the following,
Immunological (Ex: Immunoglobulin nephropathy, Lupus nephritis, Goodpasture’s disease),
Metabolic (Ex: Diabetic nephropathy),
Hemodynamic (Ex: Hypertension),
Ischemic (Ex: Shock)
Toxic (Ex: Drugs, Microbial) 39
Auto Immune Kidney Disease: Accumulation of antibodies induces a inflammatory response which is the commonest cause of kidney damage which is because of inability to perform proper auto regulation of antibodies.3
IgA Nephropathy: It was primarily explained by Berger and Hinglais in year 1968 and it is also called as “Berger’s disease” or immune-complex-mediated glomerulonephritis. Immunoglobulin (A) is found to be commonest causative feature persisting to the glomerulonephritis and as one of the leading cause of end stage renal disorders which is not linked with age factor.
Accumulation of IgA in glomerular capillaries accompanied with lesions is defined as Schönlein-Henochpurpura syndrome. Which is mostly observed in childrens with hematuria and mild proteinuria41
Lupus Nephritis: It may result from auto-antibodies (lupus erythematous) binding to circulating antigens, forming preformed immune complexes, or autoantibodies binding to antigens deposited from the circulation in the glomerular vessel walls, causing in situ immune complex formation, with initiation of an inflammatory and cytotoxic reaction.40
Goodpasture’s syndrome (GS) is a rare and organ-specific autoimmune disease that is mediated by anti-glomerular basement membrane (anti-GBM) antibodies43 and has pathology characterized by crescentic glomerulonephritis with linear immune fluorescent staining for IgG on the GBM. It typically presents as acute renal failure caused by a rapidly progressive glomerulonephritis. It was first described as a distinctive syndrome by Pasture in 1919. The disease is caused by autoantibodies against the NC1 domain of the alpha 3 chain of type IV collagen. It occurs when the immune system attacks the walls of the lungs and the tiny filtering units in the kidneys. Without early diagnosis and treatment, the disease can lead to bleeding in the lungs, kidney failure, and even death.42
DIABETIC NEPHROPATHY: It is progressive kidney disease caused by damage to the capillaries in the kidneys’ glomeruli (changes in the blood flow in the small vessels of the glomerular capsule).44It is characterized by nephrotic syndrome and diffuse scarring of the glomeruli. It is due to longstanding diabetes mellitus, and is a major reason for dialysis in many developed countries. It is classified as a small blood vessel complication of diabetes and further it leads to chronic kidney disease (CKD).45
HYPERTENSIVE KIDNEY DISEASE: It is a medical condition referring to damage to the kidney due to chronic high blood pressure. It is also known as “Hypertensive Nephropathy (HN).” HN can be divided into two types: A) Benign and B) Malignant. Benign nephrosclerosis is common in individuals over the age of 60, Whereas
Malignant nephrosclerosis is uncommon and affects 1-5% of individuals with high blood pressure, that have diastolic blood pressure passing 130 mm Hg.46The relative risk of developing ESRD is increased by up to 20 times in hypertensive patients.47
In addition, the glomerulus has a unique structure, with both an afferent and an efferent arteriole, which permits modulation of glomerular perfusion and pressure without corresponding systemic blood pressure change.48
When the force of blood flow is high, blood vessels stretch so blood flows more easily. Eventually, this stretching scars and weakens blood vessels throughout the body, including those in the kidneys. If the kidneys’ blood vessels are damaged, they may stop removing wastes and extra fluid from the body. Extra fluid in the blood vessels may then raise blood pressure even more, creating a dangerous cycle. And opposite action in hypotension.49
Drug-induced nephrotoxicity, is a major cause of acute renal failure chronic kidney disease. It occurs due to the easy availability of over-the-counter medication viz. non-steroidal anti-inflammatory drugs (NSAIDs). Antibiotics, NSAIDs, angiotensin converting enzyme inhibitors (ACEI) and contrast agents are the major drugs contributory to kidney damage.Among antibiotics especially aminoglycoside antibiotics have been the most common offending agent’s leads to chronic kidney disease. Chronic renal injury can be induced by some medications, leading to chronic tubule-interstitial inflammation, papillary necrosis or prolonged proteinuria. Drug-induced acute renal failure (ARF) accounted for 20% of all ARF.50,51Mainly anti-tubercular, anti-epileptic and chemotherapeutic agents are most responsible for the kidney damage.
Example: NSAIDs (Diclofenac Ibuprofen, Ketoprofen), Aminoglycoside antibiotics (gentamicin, amikacinesterptomycine) Amphotericin B, cyclosporine, rifampicin indinavir and more other drugs.52
What is Nephrotic syndrome?
Nephrotic syndrome is a syndrome comprising signs of nephrosis, mainly protein in the urine, low blood albumin levels, and swelling. It is a component of glomerulonephrosisin which different degrees of protein in the urine occur.53
What is Nephritic syndrome?
The nephritic syndrome is characterised by blood in the urine (especially Red blood cell casts with dysmorphic red blood cells) and a decrease in the amount of urine in the presence of hypertension. In this syndrome, inflammatory damage to cells lining the glomerulus are thought to result in destruction of the epithelial barrier, leading to blood being found in the urine.54
GLOMERULONEPHRITIS is defined as disease characterized by intraglomerular inflammation and cellular proliferation associated with hematuria. Also known as “Glomerular Nephritis.” 55
AMYLOIDOSIS is a protein-folding disease characterized by extracellular deposition of a specific soluble precursor protein that aggregates in the form of insoluble fibril.When proteins that are normally soluble in water fold to become amyloids, they become insoluble and deposit in organs or tissues, disrupting normal function.The classification of amyloidosis is based on the chemical characterization of the precursor protein. The 4 main types of systemic amyloidosis are AL, AA, ATTR, and Aβ2M type. Amyloid deposition in the kidneys can cause nephrotic syndrome, which results from a reduction in the kidney’s ability to filter proteins. The nephrotic syndrome occurs with or without elevations in creatinine and blood urea concentration.Symptoms include fluid retention, swelling, and shortness of breath.56
POLYCYSTIC KIDNEY DISEASE: It may arises sporadically as a development abnormality or may be acquired in adult life, but most forms are hereditary. Among the acquired forms simple cysts can develop in kidneys as a consequence of aging; dialysis, drugs, and hormones can cause multi cystic disease and renal cysts are often secondary manifestation of genetic proliferative syndrome. The age at onset, the severity of symptoms, and the rate of progression to end-stage renal failure or death vary widely in this group of disease.57
BIOMARKERS USED IN CKD: The bio-markers are the chemical agents which helps in detecting the kidney damage and their abnormalities detected by histology, structural abnormalities detected by imaging. 58
Biomarker Origin Outcome assessed
Urinary liver-type fatty acid-binding protein Proximal tubule Diabetic Nephropathy: Microalbuminuria and mortality
Urinary N-Acetyl-b-O-glucosaminidase Proximal tubule Diabetic Nephropathy: Albuminuria
Urinary connective tissue growth factor Proximal tubule Diabetic Nephropathy: Glomerular filtration rate decline
Interleukin-18 Tubulointerstitial Diabetic Nephropathy: Albuminuria
Apolipoprotein A-IV Intestinal enterocytes CKD: CKD Progression
Urinary CD14 mononuclear cells Polycystic kidney disease: Kidney volume
Neutrophil gelatinase associated lipocalin Proximal and distal tubule Glomerulonephritis: GFR and proteinuria CKD: CKD progression, renal replacement therapy and mortality
Kidney injury molecule-1 Proximal tubule CKD: CKD progression and renal replacement therapy
Fibroblast growth factor-23 Osteocytes and osteoblasts Diabetic Nephropathy and others CKD: CKD progression and mortality
Urinary retinol binding protein 4 Proximal tubule Congenital or acquired tubular dysfunction: Proximal tubule dysfunction
Fig-1: Biomarkers Use in Diagnosis of CKD.
Renal drug clearance: It define as hypothetical volume of body fluids from which the drugs has completely removed per unit time through the kidneys. Three processes can possibly contribute to the renal clearance of a drug: glomerular filtration, tubular secretion, and tubular reabsorption. Approximately 20–25% of cardiac output, or 1.1 L of blood per minute, goes to the kidneys. Of this volume, approximately 10% is filtered at the glomerulus. The glomerular filtration rate, i.e. the rate at which plasma water is filtered, is generally considered to be around 120 mL min−1 in a healthy adult. Large circulating molecules, such as albumin and α1-acid glycoprotein, to which many drugs are reversibly bound, are normally not filtered to any significant extent at the glomerulus. Therefore, only unbound drug in plasma water is excreted by glomerular filtration.59
Reduced renal function of patients can give rise to several problems like
Severe toxicity of drugs due to failure in proper excretion of drugs.
Due to poor elimination sensitivity to some drugs increased.
Ability to tolerate the side effects are poor in renal patients.
When renal function is poor, some of the drugs seems to be less effective.
These problems can be avoided by reducing the dose or by using alternative drugs
Dosage adjustment in patients with renal dysfunction: Adjustment of the normal drug dosage regimen may be necessary in patients with renal dysfunction to avoid excessive accumulation of the drug and/or its active metabolite(s) which leads to serious adverse reactions. A dosage regimen is characterized by the maintenance dose (DM) and the dosing interval (τ). The objective is to adjust the usual dosage regimen, by reducing the maintenance dose and/or increase the dosing interval, to avoid accumulation of the drug (and/or its active metabolites) in the patient with impaired kidney function.60
According to the level of renal function, dose of a drug must be adjusted and this depends on whether the drug is eliminated entirely by renal excretion or is partly metabolized, and how toxic it is.
Renal function is measured either in terms of Glomerular Filtration Rate (GFR) or Creatinine Clearance test
Glomerular filtration Rate (GFR) is estimated using ‘MDRD formula’ and that uses Serum Creatinine, age, sex and race and the formula is
GFR = 175 x SerumCr-1.154 × age-0.203
In females:
GFR = 175 x SerumCr-1.154 × age-0.203 × 0.742 (if female)
In blacks:
GFR = 175 x SerumCr-1.154 × age-0.203 × 1.212 (if patient is black)
CREATININE CLEARANCE TEST
Creatinine clearance can be estimated using various formulas
COCKCROFT – GAULT FORMULA
This formula is used as a marker for the estimation of Creatinine clearance “Cockcroft and Gault” are the scientist who developed this formula and it is based on Ideal Body Weight.
For Males
Creatinine Clearance = ((140-age) x Ideal Body Weight )/(Serum Creatinine Concentration)
For Females
Creatinine Clearance = ((140-age) x Ideal Body Weight )/(Serum Creatinine Concentration) x 0.85
Estimation of Ideal body weight (IBW) in kg
Male = IBW: 50 kg + 2.3 kg for each inch over 5 feet
Female = 45.5 kg + 2.3 kg for each inch over 5 feet’s.
B) JELLIFFE’S METHOD
For males: (98-[0.8](Age-20)] )/(Serum creatinine (im mg/dL) ) X (Patients BSA )/(1.78 m2 )
For females: (98-[0.8](Age-20)] )/(Serum creatinine (im mg/dL) ) x 0.9
C) SCHWATZ METHOD
Schwatz method is used to estimate GFR in children. This employs the Serum Creatinine (mg/dL), the child’s height (cm) and a constant to estimate the glomerular filtration rate:
GFR = (K x Height (in cm))/(Serum creatinine concentratio )
Here ‘K’ is a constant based on muscle mass and it varies according to the Childs age
E.g. – for babies below one year K = 0.33 for infants K=0.45 for children of age 1 to 12 years, K=0.55. In 2009 this formula was updated using a constant value for K and i.e. 0.413 and the formula is
GFR = (0.143 x Height (in cm))/(Serum creatinine concentratio )
Dosing intervals also may be different for children and adults based on their medications elimination rate. Disease states can also affect dosing in patients. Hepatic or renal dysfunction can reduce the elimination of some medications, requiring reductions in doses or dosing intervals. Gastrointestinal disease (e.g., celiac disease and gastroenteritis) may require adjustments in dosage because of altered medication absorption. Patients with cystic fibrosis and cancer may require increased dosages and decreased dosing intervals for some medications. For example, patients with cystic fibrosis may need higher doses of certain medications (e.g., theophylline, aminoglycosides, and some (3-lactam antibiotics) because of an increased total body clearance for these medications.
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