10%.
90%.
It is normocytic normochromic anaemia.
Polycystic renal disease.
Clexane.
Hypoxia.
It is used in renal impairment.
It is used in liver impairment.
Anaemia of chronic disease.
It is used in both liver and renal impairment.
Creatinine is produced by the muscles and excreted via the kidneys.
It calculates kidney function based on age, weight, and sex.
F = 1.04.
Because nicotine causes vasoconstriction, leading to increased blood pressure that can damage the kidneys.
White blood cells, red blood cells, kidney cells, or substances like protein or fat.
By the GFR from stage 1 to 5.
Creatinine and urea.
Diarrhea, bloating, wind, nausea and vomiting, stomach pain.
It reduces blood volume, leading to decreased perfusion of the kidneys.
High creatinine levels can indicate renal impairment or dehydration.
Kidney stones, calculi, tumors, or cancer.
F = 1.23.
Hypertension, smoking, dyslipidemia, obesity, and family history.
They accumulate in renal tubules, interfere with cellular processes, and can lead to cellular death.
Chronic Kidney Disease (CKD).
High levels of urea can indicate renal impairment.
Poor diabetes control.
A complication of nephrotic syndrome.
Nitrates from food (as preservatives).
Peripheral edema itself.
Suspicion of chronic kidney disease.
Decline in the GFR and urinary or structural abnormalities.
The nephron.
Urea is produced from the breakdown of proteins or amino acids, converted from ammonia by the liver.
Tiny tube-shaped particles found in urine during urinalysis.
Hypertension, diabetes, autoimmune conditions, Alport syndrome, unknown causes, acute kidney injury, and kidney stones.
It measures the concentration of solutes in urine and indicates the kidney's ability to concentrate urine.
Using the GFR.
Creatinine clearance.
Below 15 mL/min.
There is a microscopic amount of bleeding from the kidney.
Anuria, comatose states associated with liver cirrhosis, renal failure due to nephrotoxic or hepatotoxic drugs, severe hypokalaemia, severe hyponatraemia, agranulocytosis, aplastic anaemia, auditory disorder, diabetes mellitus, eosinophilia, fever, gout, haemolytic anaemia, malaise, mucosal reaction, nephritis tubulointerstitial, pancreatitis acute shock, skin eruption, tetany, and vasculitis.
Not all organisms can convert nitrates to nitrites.
Each dose should be suspended in a small quantity of water or syrup, typically ranging from 20 mL to 100 mL.
Leucocyte esterase.
Normal urine specific gravity results fall between 1.002 and 1.030.
500mg of elemental Ca2+.
About 80%.
The BUN/Cr ratio helps determine if a patient is hydrated or has acute kidney injury.
Above 90 mL/min.
Urine osmolality measures the concentration of particles in urine.
Urinary Tract Infections (UTIs).
Anuria, hypersensitivity to metolazone, hepatic coma or precoma.
They are a sign of many types of kidney diseases.
Age, weight, and sex of the individual.
Diuretics, specifically thiazides and loop diuretics.
Hypertension.
Normal results for urine osmolality are typically between 500 to 850 mOsm/kg.
Elevated urine osmolality may indicate conditions such as Addison disease, congestive heart failure, or shock.
Combine loop diuretics with thiazide diuretics.
CrCl = F (140 x Age x Weight) / Serum Creatinine (μmol/L).
Agranulocytosis, aplastic anaemia, auditory disorder, diabetes mellitus, eosinophilia, fever, gout, haemolytic anaemia, malaise, mucosal reaction, nephritis tubulointerstitial, pancreatitis acute shock, skin eruption, tetany, and vasculitis.
Loop diuretics are more effective than thiazides.
An increase in the dose results in a corresponding increase in effect.
Metolazone.
Because diabetes causes nephropathy.
It is used as an adjunct to stabilize myocytes, not specifically to manage hyperkalemia.
Hypersensitivity to salbutamol, hemodynamically significant tachycardia, hypertension, hypokalemia.
Bicarbonate ions (HCO3-).
The kidney and the liver.
Regeneration of the tubule occurs, but the patient may not return to baseline.
Possible urinary tract infections (UTIs).
Dextrose is contraindicated in diabetes, hyperglycemia, hypokalemia, peripheral edema, and pulmonary conditions.
Side effects include sweating, trembling or shaking, palpitations, and tingling lips.
Hypovolemia.
At the distal convoluted tubule.
Calcitriol (1,25-dihydroxycholecalciferol).
The kidneys fail to produce HCO3- ions, leading to an excess of H+ ions.
One gram of kayexalate contains 4.1 mEq of sodium.
Decreased appetite, arthralgia, asthenia, chest discomfort, chills, drowsiness, gastrointestinal discomfort, glycosuria, aggravated gout, haemoconcentration, hepatic disorders, hypoplastic anaemia, hypovolaemia, palpitations, peripheral neuropathy, psychotic depression, syncope, venous thrombosis, vertigo, and blurred vision.
Contraindicated in hypertension, congestive heart failure, hypokalemia, chloride loss, and metabolic alkalosis.
Side effects include bluish color, blurred vision, changes in skin color, fast or slow heartbeat, and weight gain.
Prerenal, Intrarenal, and Postrenal.
About 30 - 150 mg.
Palpitation, tachycardia, tremor, headache, muscle cramps.
Direct damage to the kidneys, such as from toxins, infections, or inflammation.
It can be administered orally or rectally as an enema.
Salt sensitive hypertension.
Escherichia coli, Lactobacillus plantarum, Neisseria gonorrhoeae, among others.
Less than 1.5L/day.
In the retroperitoneal region, behind the peritoneum.
Tamm-Horsfall proteins.
They act at different portions of the nephron and have a synergistic effect.
Full Blood Count (FBC) to check MCV and MCH.
Peripheral oedema, anaemia, osteoporosis, oliguria or anuria, metabolic acidosis, uremic encephalopathy, uremic gastritis, hyperphosphatemia.
COX enzymes.
They cause vasoconstriction, leading to high blood pressure and worsening kidney impairment.
Renal damage (nephropathy).
4 mg/min.
Heart failure, burns, dehydration, vomiting, diarrhea, internal bleeding, excessive sweating.
Hypotension reduces perfusion to the kidneys, leading to prerenal AKI.
10 - 15 mL of 10% calcium gluconate for 10 - 15 minutes.
To inhibit distal sodium reabsorption while loop diuretics block proximal sodium reabsorption.
Hypokalemia, hypersensitivity to polystyrene sulfonate resins, obstructive bowel disease, reduced gut motility.
Hyperkalemia, which can cause arrhythmia, embolism, and thrombosis leading to death.
Cortex and medulla.
Galactosemia, diabetes, GI obstructions.
Urea and creatinine.
It worsens renal impairment.
Metabolic acidosis.
Dialysis.
Prerenal AKI, Renal AKI (Intrinsic), and Post-renal AKI.
Net filtration pressure = Capillary pressure - (Bowman’s capsule pressure + Oncotic pressure).
Renal cell carcinoma and polycystic kidney disease.
Normocytic normochromic anaemia.
Decreased blood flow to the kidneys, often due to dehydration or heart failure.
There is kidney failure.
Hypoperfusion leading to ischemia.
Acute obstruction to urinary flow.
Protein in urine and RBCs in urine.
Bicarbonate.
Renal AKI.
Pale yellow or straw colored.
It is the pressure due to proteins within the Bowman’s capsule, which are negatively charged and repel the negatively charged endothelium.
Nephrotic syndrome.
Side effects include headache, muscle pain and twitching, nausea or vomiting, bradypnea, nervousness, unpleasant taste, increased frequency in urination, and increased thirst.
Build-up of urea or electrolyte imbalance.
Epilepsy, poor concentration, and pruritus (itching).
Constipation, hypertension, colitis, stomach pain, nausea and vomiting.
By administering antihistamines, preferably sedative antihistamines at night.
About 11-14 cm in length, 5-6 cm in width, and 3-4 cm in depth.
It is key in the diagnosis of kidney disease as acute or chronic.
At the thick ascending limb of the loop of Henle.
Destruction to the kidneys themselves.
From sunlight or food.
3.5 - 5.5 mmol/L.
ET-1, ET-2, ET-3.
Inactive vitamin D3.
Calcitriol, Alfacalcidol (1α-hydroxycholecalciferol), and Eldecalcitol.
The absence of urine production, defined as less than 100 mL daily.
Small urine production leads to fluid accumulation in the system.
Low oxygen perfusion to the kidney.
Normocytic normochromic anemia.
Liver disease.
In the cortex, with some descending into the medulla.
Facilitating water exchange.
Small lumen size and the presence of more angiotensin II receptors.
Endothelin causes vasoconstriction, which raises pressure and ensures high blood flow.
A form of cell signaling where a cell secretes a hormone that binds to its own surface receptors.
Kidney disease, hearing loss, and eye abnormalities.
Renal AKI.
It can suddenly drop, which is alarming.
By the afferent artery.
Skin turgor, palpitation, dry oral membranes.
The urine becomes yellowish.
It can cause cardiac issues.
By 1 - 1.5 g/dL.
It cannot return to normal.
Iron supplements and exogenous EPO.
Subcutaneous (SC).
25-hydroxycholecalciferol.
Tubular function, Endocrine function, Autocrine function.
An inherited form of kidney inflammation (nephritis) caused by a defect in a gene for collagen.
No, not all nephrotic syndrome patients respond to steroids.
Water.
There is an improvement in urine output.
It converts angiotensinogen to angiotensin I.
45 years old male.
To make a quick analysis of the urine.
Normal eGFR is ≥ 90 mL/min/1.73m².
Synthesis of Vitamin D.
Erythropoietin (EPO) deficiency.
The timing of blood indicates the source: urethra, bladder, or prostate.
Their doses are halved to prevent renal problems.
Uremia, high levels of PTH, high levels of phosphate, and accumulation of divalent ions.
Myasthenia gravis, severe renal failure, cardiac ischemia, heart block, pulmonary edema.
Diarrhea, nausea and vomiting, stomach cramps.
Blood in the urine (hematuria).
Causes water and salt retention, regulating blood pressure.
Multiple ulcers at the ankle area with hyperpigmentation and pitting bipedal edema up to the shin.
Reabsorption of about 80% of the filtrate, including glucose, Na+, amino acids, and other substances.
It combines with serum calcium to form calcium phosphate, reducing calcium levels and causing osteodystrophy.
Iron sucrose is complexed with sucrose, while iron dextran is complexed with a carbohydrate polymer derived from dextran.
H+ ions move into the intracellular space, displacing K+ ions into the blood, resulting in hyperkalemia.
They can cause a build-up of fluids, worsening the condition.
The fractional excretion of sodium (F eNa).
The cortex (outer portion) and the medulla (conical region).
F eNa = (Urine Na / Serum Na x Serum Cr / Urine Cr) x 100%.
Nitrogenous compounds and other toxins.
It is attached to the afferent artery and plays a role in regulating blood pressure and filtration.
They can cause renal dysfunction due to a drop in renal perfusion pressure and decrease in glomerular filtration.
Acute Kidney Injury (Septic ATN) from UTI and CKD secondary to chronic Glomerular Nephritis.
Oxygen depletion or fluid depletion.
Dizziness, nausea, and weakness.
It is caused by the buildup of urea in CKD patients, leading to ulceration and bleeding.
It causes natriuresis and allows renal blood flow.
Prostaglandin H2 (PGH2).
The remaining 20% of the filtrate.
1α hydroxylase.
Low urine output, less than 400 mL per day or 20 mL per hour.
A sudden reduction in kidney function within 48 hours.
Food, medications, and other conditions.
It results in a deficit in hydrostatic pressure gradient (HPG), indicating reduced kidney function or filtration.
Impairment of perfusion.
Proton pump inhibitors (PPIs) are typically used.
They cause vasodilatation and ensure renal blood flow.
It becomes lesser than that of the filtrate, causing water to move in the reverse direction.
Obstruction of urine flow, such as from kidney stones or enlarged prostate.
Endothelin receptor A (ET A) and B (ET B).
They cause direct injury to the renal tubules, impairing kidney function.
It can be hydroxylated at C-1 before reaching the liver.
The Bowman’s capsule and the glomerulus.
Hypovolemia and fluid overload.
Renin-Angiotensin-Aldosterone System (RAAS).
Diabetes mellitus.
Parenteral iron, such as iron sucrose or iron dextran.
Always 10 mmHg, which contributes to ultrafiltration.
Oliguria phase, characterized by a reduction in urine output.
About 7 to 14 days.
Reabsorption of nutrients, excretion of waste, fluid balance, and pH regulation.
Because H+ ions come from all metabolic activities in the body.
Hyperkalemia, severe normocytic anemia, and hypertension.
A condition that causes injury before reaching the kidney, often due to reduced blood flow.
It implies glomerular damage.
Dehydration.
They cause pronounced vessel dilation in the efferent artery compared to the afferent artery.
It is the buildup of phosphate due to impaired excretion by the kidneys.
Other prostaglandins such as PGE2, which causes diuresis.
99%.
Causes vasoconstriction and the release of aldosterone.
Increased production of RBCs, which raises blood viscosity.
A condition where large proteins leak into urine due to podocyte damage.
To cause increased pressure and allow enough time for filtration.
High PTH suppresses RBC production.
Exchange of electrolytes, but no water exchange.
Typically administered as a slow IV infusion.
10 - 12 g/dL, or 10 - 13 g/dL for patients with diabetes.
They cause preferential vasodilation, impairing the kidney's ability to compensate for low perfusion states.
A hormone produced by the kidneys that stimulates red blood cell production.
Acute interstitial nephritis, potentially leading to acute kidney injury.
Due to edema around the GIT, which reduces iron absorption.
Peripheral edema, ascites, hypertension, congestive heart failure, uremia, encephalopathy, hyperphosphatemia.
It cannot differentiate between RBCs and Hb/myoglobin.
It indicates that the kidney is in end-stage disease.
The efferent artery has more angiotensin II receptors than the afferent artery, influencing pressure and filtration.
COX-1 (constitutive) and COX-2 (inducible).
Increased volume of urine.
Intravascular volume and intravascular pressure.
Encephalopathy.
The amount of filtrate that leaves the glomerulus per unit time.
The patient may develop antibodies leading to pure red blood cell aplasia.
Iron sucrose has a lower risk of severe allergic reactions compared to iron dextran.
Scanning, imaging, or biopsy.
