Nephrology, kidney Disease, bladder Cancer,Acute Renal Failure,Chronic Kidney Disease

1. Nephrology
Dr. Anam Nazeer
Pharm-D, Bsc, M.phil Pharmacology,Rph
Dr. Mohsan Suhail
MBBS.FCPS
◦ Rashid Latif Medical Complex

2. Contents
◦ Introduction
◦ Types of Kidney diseases
◦ Bladder Cancer
◦ Acute Renal Failure
◦ Chronic Renal Failure

3. Nephrology
Nephrology is a branch of
medical science that deals with
diseases of the kidneys.
Nephrology (from Greek
nephros "kidney", combined
with the suffix -logy, "the
study of") is a specialty of
medicine and pediatrics that
concerns itself with the study
of normal kidney function,
kidney problems, the treatment
of kidney problems and renal
replacement therapy (dialysis
and kidney transplantation).

7. Nephron
◦ Nephron, functional unit of the kidney, the structure that actually produces urine in the process of
removing waste and excess substances from the blood. There are about 1,000,000 nephrons in each
human kidney.
◦ nephron of the kidney Each nephron of the kidney contains blood vessels and a special tubule. As the
filtrate flows through the tubule of the nephron, it becomes increasingly concentrated into urine. Waste
products are transferred from the blood into the filtrate, while nutrients are absorbed from the filtrate into
the blood.

8. FUNCTION OF KIDNEYS
◦ The kidneys are a pair of fist-sized organs located at the bottom of the rib cage. There is one
kidney on each side of the spine.
◦ Kidneys are essential to having a healthy body. They are mainly responsible for filtering waste
products, excess water, and other impurities out of the blood. These toxins are stored in the
bladder and then removed during urination. The kidneys also regulate pH, salt, and potassium
levels in the body. They produce hormones that regulate blood pressure and control the
production of red blood cells. The kidneys even activate a form of vitamin D that helps the body
absorb calcium.

9. FUNCTION OF KIDNEYS
◦ Forming and Eliminating Urine
◦ Maintaining blood volume with proper balance of water, electrolytes, and pH.
◦ Retaining key compounds such as glucose, while excreting wastes such as urea.
◦ Controlling Arterial Blood Pressure
◦ Regulating Erythrocyte Development

10. FORMATION OF URINE
◦ FORMATION OF URINE
◦ The kidneys filter unwanted substances from the blood and produce urine to excrete them.
There are three main steps of urine formation: glomerular filtration, reabsorption, and secretion.
These processes ensure that only waste and excess water are removed from the body.
◦ Glomerular Filtration
◦ Reabsorption
◦ Secretion

11. Kidney Diseases
◦ Kidney disease affects approximately 26 million American adults. It occurs when your kidneys
become damaged and can’t perform their function.
◦ Damage may be caused by diabetes, high blood pressure, and various other chronic (long-
term) conditions. Kidney disease can lead to other health problems, including weak bones, nerve
damage, and malnutrition.

12. types kidney disease
◦ Chronic kidney disease
◦ Nephrotic Syndrome
◦ Renal Failure
◦ Bladder Cancer
◦ Kidney stones
◦ Glomerulonephritis
◦ Polycystic kidney disease
◦ Urinary tract infections

13. Bladder cancer
◦ Bladder cancer is the rapid, uncontrolled growth of abnormal cells in the bladder.
◦ Cancer usually begins in the lining of the bladder.
◦ The cancerous cells may spread through the lining into the muscular wall of the bladder.
◦ CAUSES: The cause of is not known Changes in the genetic material (DNA) of bladder cells may
play a role.
◦ Chemicals in the environment and cigarette smoking.

14. ◦ When the lining of the bladder is irritated for a long time, cell changes that lead to cancer may
occur Other causes may be like radiation treatment, having catheters in place for a long time, or
having the parasite that causes schistosomiasis.

15. SYMPTOMS
◦ SYMPTOMS: Blood or blood clots in the urine (hematuria)
◦ Pain during urination (dysuria)
◦ Urinating small amounts frequently.
◦ Frequent urinary tract infections (UTIs)
◦ Pain in the lower back around the kidneys (flank pain).
◦ Swelling in the lower legs.
◦ A growth in the pelvis near the bladder (pelvic mass

16. STAGES OF BLADDER CANCER
◦ : There are four stages of bladder cancer, stages 0 to IV:
◦ Stage 0: Cancer cells are only on the surface of the inner layer of the bladder. This may be
called carcinoma in situ.
◦ Stage I: Cancer has grown deeper into the inner layer but not into the muscle layer.
◦ Stage II: Cancer has grown into the muscle layer of the bladder. –.

17. STAGES OF BLADDER CANCER
◦ Stage III: Cancer has grown through the muscle layer and into nearby organs, such as the
prostate, uterus, or vagina.
◦ Stage IV: Cancer has grown into the wall of the pelvis or the belly but not into any lymph
nodes. Or the cancer has spread into at least one lymph node or to another part of the body,
such as the liver, lungs, or bones

18. TREATMENT
◦ TREATMENT: Surgery to remove the cancer.
◦ Chemotherapy to destroy cancer cells using medicines.
◦ Radiation therapy to destroy cancer cells using high-dose X-rays or other high-energy rays.
◦ Immunotherapy. This treatment causes your body's natural defenses, known as your immune
system, to attack bladder cancer cells

19. Acute renal failure
◦ Acute Renal failure;- is a sudden and usually
reversible decrease in the glomerular
filtration rate (GFR) occurring over a period
of hours to days.
◦ Acute renal failure (ARF) is broadly defined
as a decrease in glomerular filtration rate
(GFR) occurring over hours to weeks that is
associated with an accumulation of waste
products, including urea and creatinine.
◦ A combination of the serum creatinine (Scr)
value with change in either Scr or urine
output (UOP) as the primary criteria for
diagnosing ARF.

20. Pathophysiology
◦ ARF can be categorized as
◦ Prerenal (resulting from decreased renal perfusion),
◦ Intrinsic (resulting from structural damage to the kidney),
◦ Postrenal (resulting from obstruction of urine flow from the renal tubule to the urethra),
◦ Functional (resulting from hemodynamic changes at the glomerulus independent of
decreased perfusion or structural damage).

21. Symptoms
◦ Signs and symptoms of acute kidney failure may include:
◦ Decreased urine output, although occasionally urine output remains normal
◦ Fluid retention, causing swelling in your legs, ankles or feet
◦ Shortness of breath
◦ Fatigue
◦ Confusion
◦ Nausea
◦ Weakness
◦ Irregular heartbeat
◦ Chest pain or pressure
◦ orthostatic hypotension
◦ Seizures or coma in severe cases

22. Diagnosis
◦ Thorough medical and medication histories, physical examination, assessment of laboratory
values and if needed, imaging studies, are important in the diagnosis of ARF.
◦ Scr and blood urea nitrogen cannot be used alone to diagnose ARF because they are insensitive
to rapid changes in GFR and therefore may not reflect current renal function.
◦ Monitoring changes in UOP can help diagnose the cause of ARF.
◦ Acute anuria (less than 50 mL urine/day) is secondary to complete urinary obstruction or a
catastrophic event (e.g., shock).
◦ Oliguria (400 to 500 mL urine/day) suggests prerenal azotemia.

23. ◦ Nonoliguric renal failure (more than 400 to 500 mL urine/day) usually results from acute intrinsic
renal failure or incomplete urinary obstruction.
◦ Urinalysis can help clarify the cause of ARF. Certain laboratory parameters are helpful in the
assessment of renal function with ARF.
◦ Urine microscopy gives further information to assist with determination of the etiology of the
ARF.

24. TREATMENT
◦ PREVENTION OF ACUTE RENAL FAILURE • Risk factors for ARF include advanced age, acute
infection, preexisting chronic respiratory or cardiovascular disease, dehydration, and chronic
kidney disease (CKD).
◦ Decreased renal perfusion secondary to abdominal or coronary bypass surgery, acute blood
loss in trauma, and uric acid nephropathy also increase risk.
◦ Nephrotoxin administration (e.g., radio contrast dye) should be avoided whenever possible.
◦ When patients require contrast dye and are at risk of contrast dye–induced nephropathy, renal
perfusion should be maximized through strategies such as assuring adequate hydration with
normal saline or sodium bicarbonate solutions and administration of oral acetylcysteine 600
mg every 12 hours for four doses.

25. ◦ Strict glycemic control with insulin in diabetics has also reduced the development of ARF.
◦ Amphotericin B nephrotoxicity can be reduced by slowing the infusion rate to 24 hours .
◦ Many other strategies are popular but lack supportive evidence, including mannitol, loop
diuretics, dopamine, and fenoldopam.

26. MANAGEMENT OF ESTABLISHED
ACUTE RENAL FAILURE
◦ Nonpharmacologic Approaches
◦ Supportive care goals include maintenance of adequate cardiac output and blood pressure to
optimize tissue perfusion while restoring renal function to pre-ARF baseline.
◦ Medications associated with diminished renal blood flow should be stopped. Appropriate fluid
replacement should be initiated.
◦ Avoidance of nephrotoxins is essential in the management of patients with ARF.
◦ Renal replacement therapy (RRT), such as hemodialysis and peritoneal dialysis, maintains fluid and
electrolyte balance while removing waste products.

27. ◦ Intermittent RRT (e.g., hemodialysis) has the
◦ advantage of widespread availability and the convenience of lasting only 3 to 4 hours.
◦ Disadvantages include difficult venous dialysis access in hypotensive patients and hypotension due
to rapid removal of large amounts of fluid. •
◦ Several continuous renal replacement therapy (CRRT) variants have been developed.
◦ CRRT, performed as continuous hemodialysis, continuous hemofiltration, or both, is becoming
increasingly popular.
◦ CRRT gradually removes solute resulting in better tolerability by critically ill patients.
◦ Disadvantages include limited availability, need for 24-hour nursing care, high expense, and
incomplete guidelines for drug dosing

28. Pharmacologic Approaches
◦ •Loop diuretics have not been shown to accelerate ARF recovery or improve patient outcome;
however, diuretics can facilitate management of fluid overload.
◦ The most effective diuretics are mannitol and loop diuretics.
◦ • Mannitol 20% is typically started at a dose of 12.5 to 25 g IV.
◦ Disadvantages include IV administration, hyperosmolality risk, and need for monitoring
because mannitol can contribute to ARF.
◦ Equipotent doses of loop diuretics (furosemide, bumetanide, torsemide, ethacrynic acid) have
similar efficacy.

29. ◦ Ethacrynic acid is reserved for sulfaallergic patients.
◦ Continuous infusions of loop diuretics appear to be more effective and to have fewer adverse
effects than intermittent boluses.
◦ An initial IV loading dose (equivalent to furosemide 40 to 80 mg) should be administered before
starting a continuous infusion (equivalent to furosemide 10 to 20 mg/hour).
◦ Strategies are available to overcome diuretic resistance, a common problem in patients with ARF.
◦ Agents from different pharmacologic classes, such as diuretics that work at the distal convoluted
tubule (thiazides) or the collecting duct (amiloride, triamterene, spironolactone), may be
synergistic when combined with loop diuretics.
◦ Metolazone is commonly used because, unlike other thiazides, it produces effective diuresis at
GFR less than 20 mL/min

30. ELECTROLYTE MANAGEMENT AND
NUTRITION THERAPY
◦ Hyperkalemia is the most common and serious electrolyte abnormality in ARF. Typically, potassium
must be restricted to less than 3 g/day and monitored daily.
◦ Hypernatremia and fluid retention commonly occur, necessitating restricting daily sodium intake to
no more than 3 g.
◦ All sources of sodium, including antibiotics, need to be considered when calculating daily sodium
intake.
◦ Phosphorus and magnesium should be monitored; neither is efficiently removed by dialysis.
◦ Enteral , but not parenteral, nutrition has been shown to improve patient outcomes.

32. Chronic Kidney Disease
◦ Chronic kidney disease (CKD) is a progressive loss of function over several months to years,
characterized by gradual replacement of normal kidney architecture with interstitial fibrosis.
◦ • CKD is categorized by the level of kidney function, based on glomerular filtration rate (GFR),
into stages 1 to 5, with each increasing number indicating a more advanced stage of the
disease, as defined by a declining GFR.

35. ◦ This classification system from the National Kidney Foundation’s Kidney Dialysis Outcomes and
Quality Initiative (K/DOQI) also accounts for structural evidence of kidney damage.
◦ • CKD stage 5, previously referred to as end--stage renal disease (ESRD), occurs when the
GFR falls below 15 mL/min per 1.73 m2 body surface area. The patient with stage 5 CKD
requiring chronic dialysis or renal transplantation for relief of uremic symptoms is said to have
ESRD.

37. Pathphysiology
◦ Susceptibility factors increase the risk for kidney disease but do not directly cause kidney
damage. Susceptibility factors include advanced age, reduced kidney mass and low birth
weight, family history, low income or education, systemic inflammation, and dyslipidemia.
◦ • Initiation factors initiate kidney damage and can be modified by drug therapy. Initiation
factors include diabetes mellitus, hypertension, autoimmune disease, polycystic kidney
disease, and drug toxicity.
◦ • Progression factors hasten decline in kidney function after initiation of kidney damage.
Progression factors include glycemia in diabetics, hypertension, proteinuria, and smoking.

38. Risk Factors

39. Sign and symptoms
◦ CKD development and progression is insidious. Patients with stage 1 or 2 CKD usually do not
have symptoms or metabolic derangements seen with stages 3 to 5, such as
◦ anemia,
◦ secondary hyperparathyroidism,
◦ cardiovascular disease,
◦ malnutrition,
◦ fluid and electrolyte abnormalities that are more common as kidney function deteriorates.

40. ◦ • Uremic symptoms
◦ fatigue,
◦ weakness,
◦ shortness of breath,
◦ mental confusion,
◦ nausea, vomiting,
◦ bleeding,
◦ Anorexia are generally absent in stages 1 and 2, minimal during stages 3 and 4, and common in
patients with stage 5 CKD who may also experience itching, cold intolerance, weight gain, and
peripheral neuropathies.

41. Diagnosis

42. Non-Pharmacological Therapy
◦ A low-protein diet (0.6 to 0.75 g/kg/day) can delay progression of CKD in patients with or
without diabetes, although the benefit is relatively small.

43. Pharmacological Therapy
◦ Hyperglycemia
◦ • Intensive therapy in patients with type 1 and type 2 diabetes reduces microvascular
complications, including nephropathy. Intensive therapy can include insulin or oral drugs and
involves blood sugar testing at least three times daily.
◦ • The progression of CKD can be limited by optimal control of hyperglycemia and
hypertension.

44. Hypertension
◦ • Adequate blood pressure control can reduce the rate of decline in GFR and albuminuria in
patients with or without diabetes.
◦ • Antihypertensive therapy should be initiated in diabetic or nondiabetic CKD patients with an
angiotensin-converting enzyme inhibitor (ACEI) or an angiotensin II receptor blocker.
Nondihydropyridine calcium channel blockers are generally used as second-line
antiproteinuric drugs when ACEIs or angiotensin II receptor blockers are not tolerated.

45. ◦ ACEI clearance is reduced in CKD, therefore treatment should begin with the lowest possible
dose followed by gradual titration to achieve target blood pressure and, secondarily, to
minimize proteinuria.
◦ No individual ACEI is superior to another.
◦ • GFR typically decreases 25% to 30% within 3 to 7 days after starting ACEIs because this class
reduces intraglomerular pressure. Sustained increases in the serum creatinine by more than
30% after starting ACEIs may be due to the ACEI and discontinuation should be strongly
considered. Serum potassium should also be monitored to detect development of
hyperkalemia after initiating or increasing the dose of an ACEI.

46. Supportive Therapies
◦ • Dietary protein restriction lipid-lowering medications, smoking cessation, and anemia
management may help slow the rate of CKD progression.
◦ • The primary goal of lipid-lowering therapies in CKD is to decrease the risk for progressive
atherosclerotic cardiovascular disease
◦ • A secondary goal is to reduce proteinuria and renal function decline seen with
administration of statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors).

47. Fluid and electrolyte abnormalities
◦ Serum sodium concentration is generally maintained by an increase in fractional
excretion of sodium, resulting in a volume-expanded state. The most common
manifestation of increased intravascular volume is systemic hypertension.
◦ • The kidney’s ability to adjust to abrupt changes in sodium intake is diminished in
patients with ESRD. Sodium restriction beyond a no-added salt diet is not
recommended unless hypertension or edema is present. A negative sodium
balance can decrease renal perfusion and cause a further decline in GFR.
◦ • Diuretic therapy or dialysis may be necessary to control edema or blood
pressure.

48. Refrences
◦ DiPiro JT. Encyclopedia of Clinical Pharmacy. 1st Ed. Informa Healthcare; 2002.
◦ DiPiro JT. Pharmacotherapy: A Pathophysiologic Approach. McGraw Hill Companies, South
Carolina; 2008
◦ Rantucci MJ. Pharmacists Talking with Patients: A Guide to Patient Counseling. 2nd Ed.
Lippincott Williams & Wilkins; 2006