Aula 8 - Renal Disease Flashcards
1
Q
What are the main types of acute renal failure?
A
- Pre-renal: Reduced blood flow to the kidneys.
- Renal (intrinsic): Direct damage to the renal parenchyma.
- Post-renal: Obstruction of urinary flow.
2
Q
What arteries enter the kidneys through the hilum?
A
The renal arteries branch off from the aorta to supply oxygenated blood to the kidneys. The right renal artery supplies blood to the right kidney, and the left renal artery supplies blood to the left kidney.
3
Q
How is the kidney structurally divided internally?
A
Internally, the kidney is divided into the renal cortex (outer layer), renal medulla (inner layer), renal pyramids, renal columns, calyces (minor and major), and renal pelvis.
4
Q
What is the function of the renal cortex and medulla?
A
The renal cortex contains glomeruli and is where filtration begins, while the renal medulla contains renal pyramids that help concentrate urine and transport it to the calyces.
5
Q
What is the renal pelvis and what does it do?
A
The renal pelvis is a funnel-shaped structure that collects urine from the major calyces and passes it into the ureter for transport to the bladder.
6
Q
What structures are involved in the flow of urine from the nephron to the ureter?
A
Urine flows from the nephron → renal papilla → minor calyx → major calyx → renal pelvis → ureter
7
Q
What are renal pyramids and where are they located?
A
Renal pyramids are cone-shaped structures found in the medulla. They contain tubules (i.e., the loops of Henle and collecting ducts), which allow to concentrate and transport urine to the renal papillae.
8
Q
Match the part of the nephron to its function.
Parts:
A. Glomerulus
B. Proximal Convoluted Tubule
C. Loop of Henle
D. Distal Convoluted Tubule
E. Collecting Duct
Functions:
a. Filtration of blood, allowing water and small molecules to pass through.
b. Selective reabsorption of water, sodium, and other ions.
c. Reabsorption of water, concentrating urine.
d. Further modification of filtrate, including secretion of waste.
e. Collection and final adjustment of urine concentration before excretion.
A
- A) a
- B) b
- C) c
- D) d
- E) e
9
Q
A patient presents with a kidney disease that affects the filtration barrier of the glomerulus. What would likely be the result of this condition?
A. Increased filtration of proteins into the urine
B. Decreased secretion of waste products
C. Increased water reabsorption
D. Decreased production of urine
A
A. Increased filtration of proteins into the urine
When the glomerular filtration barrier is damaged, it may allow proteins like albumin to leak into the urine, a condition called proteinuria.
10
Q
What are the main renal functions?
A
- Excretion of metabolites (urea, ammonia, uric acid, organic acids/bases) through blood filtration
- Hydro-electrolyte balance (change in urine composition)
- Acid-base (pH) balance (change in urine composition)
- Regulation of blood pressure (through increase or decrease in volemia)
- Endocrine secretion (erythropoietin, vitamin D, renin)
11
Q
What is the main function of the renal corpuscle?
(part of the nephrons)
A
Generate the glomerular filtrate, composed by water, ions, and small molecules
12
Q
What is the main function of the proximal convoluted tubule?
(part of the nephrons)
A
It reabsorbs sodium chloride, potassium, water, glucose, amino acids, bicarbonate, calcium and phosphate, and secretes amonium and creatinine.
13
Q
What is the main function of thin descending limb of the loop of Henle?
(part of the nephrons)
A
Water reabsorption
14
Q
What is the main function of thin ascending limb of the loop of Henle?
(part of the nephrons)
A
Sodium and chloride reabsorption
15
Q
What is the main function of thick ascending limb of the loop of Henle?
(part of the nephrons)
A
Amonium, sodium and chloride reabsorption
16
Q
What is the main function of the distal convoluted tube?
(part of the nephrons)
A
Sodium and chloride reabsorption
17
Q
What is the main function of collecting duct?
(part of the nephrons)
A
Reabsorbs sodium, chloride and water, and secretes amonium, hydrogen ions and potassium
18
Q
Glomerular filtration rate (GFR) reflects the ________ of functional nephrons
A
quantity
19
Q
Explain the RAA system in blood pressure regulation.
A
When there is a low perfusion pressure in the kidneys (indicading low arterial blood pressure), they produce renin, which converts the angiotensinogen (produced by the liver and circulating in the blood stream) into angiotensin I. Then, in the lungs, the angiotensin converting enzyme (ACE) converts angiotension I into angiotensin II, which promotes arteriolar vasoconstriction, as well as the secretion of ADH (antidiuretic hormone) by the pituary gland and aldosterone (mineralocorticoid steroid hormone) by the adrenal glands that increase water reabsorption in the kidney, in order to increase blood volemia and, consequently, increase blood pressure.
20
Q
Indicate and explain each of the 4 hydrostatic and osmotic pressures that influence glomerular filtration.
A
- Hydrostatic Pressure in the Glomerular Capillaries (Pc): the pressure exerted by blood inside the glomerular capillaries is the main force pushing fluid out of the capillaries and into the Bowman’s capsule.
- Hydrostatic Pressure in the Bowman’s Space (Pb): this is the pressure exerted by the filtrate already inside the Bowman’s capsule.
- Osmotic Pressure in the Glomerular Capillaries (πc): this pressure is created by the proteins (mainly albumin) that remain in the blood. These proteins draw water back into the glomerular capillaries.
- Osmotic Pressure in the Bowman’s Space (πb): this is usually negligible, as proteins are not typically found in the Bowman’s space.
21
Q
The glomerular filtration rate (GFR) is the rate at which the kidneys filter blood, and it is influenced by the balance of the ____________ and ________ pressures, as well as by the ________ in the afferent and efferent arterioles.
A
hydrostatic, osmotic, resistance
22
Q
What happens to the glomerular filtration rate (GFR) when there is a vasoconstriction of the afferent arteriole in the glomerulus?
A
Constriction of the afferent arteriole reduces blood flow into the glomerulus, decreasing the hydrostatic pressure in the glomerular capillaries (Pc) and thus reducing the GFR.
23
Q
What happens to the glomerular filtration rate (GFR) when there is a vasoconstriction of the efferent arteriole in the glomerulus?
A
Constriction of the efferent arteriole increases hydrostatic pressure within the glomerulus (hydrostatic pressure in the glomerular capillaries, Pc), which can increase the GFR, while dilation of the efferent arteriole decreases GFR.
24
Q
A patient with hypertension is prescribed a medication that causes constriction of the afferent arteriole. What would be the effect on their glomerular filtration rate (GFR)?
A. Increase GFR
B. Decrease GFR
C. No change in GFR
D. Increase osmotic pressure in Bowman’s space
A
B. Decrease GFR
Constriction of the afferent arteriole reduces blood flow into the glomerulus, lowering the hydrostatic pressure and reducing the GFR.
25
What is the effect of an increase in osmotic pressure in the glomerular capillaries (πGC) on the glomerular filtration rate (GFR)?
A. Increase GFR
B. Decrease GFR
C. No change in GFR
D. It is irrelevant to GFR
**B. Decrease GFR**
An increase in osmotic pressure in the glomerular capillaries would attract more water into the capillaries, reducing the amount of filtrate formed and thus decreasing the GFR.
26
Why does glomerular filtration rate (GFR) increase with resistance in the efferent arteriole up to a certain point, then decrease despite further resistance?
Initially, increased resistance in the efferent arteriole raises glomerular hydrostatic pressure (because the blood cannot leave as easily), promoting filtration (as it pushes fluid out of the capillaries and into the Bowman’s capsule) and, thus, increasing GFR.
However, at high resistance, the body compensates by raising the pressure to maintain filtration, leading to higher resistance in the afferent arteriole. This leads to a decrease in blood flow entering the glomerulus, reducing perfusion and eventually decreasing GFR.
27
What physiological parameters can be measured to evaluate kidney function?
* Glomerular Filtration Rate
* Urea-Creatinine Ratio
* Urinary Osmolarity
* Fraction of sodium excreted in the urine
28
What imaging techniques can be used to assess kidney function?
* Ultrasound
* Computerised tomography (CT)
* Magnetic Resonance Imaging (MRI)
* Radiography
29
How can we estimate the glomerular filtration rate?
We can't measure GFR directly, but we can estimate it through the **Creatinine clearance method** and/or applying **estimation equations**.
1. Creatinine is a byproduct of muscle metabolism and is filtered freely by the glomerulus. It is neither reabsorbed nor significantly secreted, making it a reliable marker for kidney function. **Creatinine clearance is an estimate of GFR because it reflects the volume of plasma cleared of creatinine per minute**. It can be calculated by measuring the concentration of creatinine in urine and blood.
2. Based on serum creatinine, we can also apply the following equations:
* **Cockcroft-Gault Equation**: estimates kidney function based on age, weight, and serum creatinine levels, but it may overestimate GFR in patients with normal kidney function.
* **MDRD (Modification of Diet in Renal Disease) Equation**: widely used in clinical settings and adjusts for race and sex, but tends to underestimate GFR in patients with higher GFR.
* **CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration)**: this equation is considered more accurate than MDRD, especially in those with normal or mildly reduced GFR. It uses age, sex, race, and serum creatinine levels to estimate GFR.
30
What is the normal Urea-Creatinine Ratio?
40-110:1
31
The accumulation of nitrogen products (urea and creatinine) in the blood is called ________ and reflects a ________ (high/low) glomerular filtration rate.
azotemia, low
32
How can azotemia be classified according to the origin of the renal lesion? What are the urea-creatinine ratio values associated with each type?
* Pre-renal (U/Cr > 110:1)
* Intra-renal (U/Cr < 40:1, but U and Cr are both elevated)
* Post-renal (normal U/Cr, of 40:110:1)
33
What are the main parameters to analyze in urine?
Appearance, color, density, and composition, concentration and volume.
34
What is the normal osmolarity (concentration of solute) range for urine?
500-850 mOsm/kg
35
The normal range for osmolarity of urine is 500-850 mOsm/kg. When osmolarity of urine is < 350 mOsm/kg, it indicates ________ (pre-renal dysfunction/intra-renal dysfunction).
intra-renal dysfunction
36
What is the normal urine volume per day?
400 to 2500 mL/day, depending on fluid intake
37
What is polyuria?
Polyuria refers to a high urine output, with a volume of urine usually > 2500 mL/day.
38
What is oliguria?
Oliguria refers to a low urine output, with a volume of urine usually < 400 mL/day.
39
What is anuria?
Anuria is nonpassage of urine, with an urine volume < 100 mL/day or absence of urination.
40
What is pollakiuria?
Increased frequency of urination
41
What is nocturia?
The urge to urinate during the night.
42
What is dysuria?
Pain or difficulty when urinating.
43
Renal failure is characterized by an ________ (increased/normal/decreased) glomerular filtration rate.
decreased
44
What are the two main types of renal failure?
Acute kidney injury (AKI) and chronic kidney disease (CKD).
45
What is acute kidney injury (AKI)?
A rapid decline in kidney function over hours to days, often reversible if treated promptly.
46
What is chronic kidney disease (CKD)?
A progressive and irreversible loss of kidney function over months to years.
47
What percentage of acute kidney injury cases are due to pre-renal causes?
About 60%
48
What percentage of acute kidney injury cases are due to intra-renal causes?
About 35%
49
What percentage of acute kidney injury cases are due to post-renal causes?
About 5%
50
What are the three main causes of renal failure?
* Pre-renal causes: reduction in kidney perfusion.
* Intra-renal causes: damage to the kidney tissues.
* Post-renal causes: obstruction of urine flow.
51
What is renal failure?
Renal failure is the inability of the kidneys to adequately filter waste products and maintain fluid, electrolyte, and acid-base balance, i.e., to maintain their normal functions.
52
Pre-renal failure occurs when there is a reduction in ________ in the kidneys and/or ________ (low/high) glomerular filtration rate.
perfusion, low
53
Intra-renal failure involves direct ________ to kidney tissues.
damage
54
Post-renal failure is caused by ________ of urine flow.
obstruction
55
What is the main mechanism behind pre-renal failure?
The central mechanism is a reduction in the distribution of blood to the kidney, which compromises renal filtration capacity.
56
How does heart failure lead to pre-renal failure?
Reduced cardiac output decreases blood volume and blood pressure, including in the renal artery, which decreases renal perfusion.
57
How does renal artery stenosis affect GFR and cause pre-renal failure?
Narrowing of the renal artery reduces blood flow, lowering glomerular filtration pressure and, thus, GFR, leading to pre-renal failure.
58
How does sepsis cause pre-renal failure?
Systemic vasodilation (due to inflammatory response) and consequent hypotension reduce renal artery pressure and renal perfusion.
59
How do hemorrhage, vomiting, or diarrhea contribute to pre-renal failure?
They cause hypovolemia, lowering blood pressure and renal perfusion.
60
How does dehydration contribute to pre-renal failure?
Dehydration causes a decreased blood volume, which reduces renal artery blood flow and pressure, decreasing renal perfusion and GFR.
61
How do NSAIDs contribute to pre-renal failure?
NSAIDs inhibit prostaglandin synthesis (D2 and E2) - hormone-like substances that promote inflammation - reducing afferent arteriole vasodilation, which lowers glomerular capillary pressure and GFR.
62
How do Angiotensin-converting enzyme (ACE) inhibitors cause pre-renal failure?
ACE is the enzyme responsible for converting angiotensin I in angiotensin II, which induces arteriole vasoconstriction. Therefore, ACE inhibitors reduce angiotensin II, which normally constricts the efferent arteriole. Less constriction (aka less resistance) leads to decreased glomerular pressure (since blood can flow out without resistance) and GFR.
63
How does hypercalcemia contribute to pre-renal failure?
Hypercalcemia can result when too much calcium enters the extracellular fluid (e.g., blood) or when there is insufficient calcium excretion from the kidneys.
Calcium induces smooth muscle contraction and, therefore, causes induces afferent arteriole vasoconstriction. This reduces blood flow to the glomerulus, reducing glomerular capillary pressure, reducing hydrostatic pressure and, thus, reducing GFR.
Calcium also reduces reabsorption of sodium, chloride, and water in the Henle loop, so more fluid stays in the urine, and less is retained in the body, leading to fluid loss which contributes to hypovolemia, reducing renal artery pressure and renal perfusion.
64
T/F: NSAIDs reduce GFR by increasing afferent arteriole vasodilation.
False. NSAIDs decrease vasodilation, leading to vasoconstriction and lower GFR.
65
T/F: ACE inhibitors decrease efferent arteriole resistance.
True. They inhibit angiotensin II, causing vasodilation of the efferent arteriole.
66
NSAIDs inhibit ________, leading to reduced afferent arteriole vasodilation.
prostaglandins (D2 and E2)
67
ACE inhibitors reduce levels of ________, causing dilation of the efferent arteriole.
angiotensin II
68
Hypovolemia leads to decreased ________, resulting in lower GFR.
renal artery pressure
69
A 75-year-old male presents with hypotension and recent vomiting. Labs show increased serum creatinine.
**What is the likely cause of his acute renal failure?**
Pre-renal failure due to hypovolemia from fluid loss (vomiting) and hypotension, leading to decreased renal perfusion.
* Vomiting → fluid loss → ↓ intravascular volume → hypotension → ↓ renal perfusion pressure → ↓ glomerular filtration → ↑ serum creatinine
70
What are the two main causes of intra-renal failure?
* Glomerulopathies
* Tubulointerstitial diseases
71
What are the 4 main manifestations of glomerulopathies?
* Hematuria (blood in urine)
* Proteinuria (proteins in urine)
* Decreased glomerular filtration rate
* Hypertension
72
What are the two main types of glomerulopathies?
* Nephrotic syndrome
* Nephritic syndrome
73
What is nephrotic syndrome?
It's a condition that causes the deposition of proteins in unknown autoimmune context or context that damage the filtration membrane.
74
What is nephritic syndrome?
Damaging inflammatory response to a bacterial or viral infection that damages the filtration membrane.
75
What are the main bacterial and viral infections that lead to nephritic syndrome?
Bacterial infections:
* Pharyngitis
* Streptococcal tonsillitis
* Bacterial endocarditis
* Infectious cellulitis
Viral infections:
* Hepatitis B and C
76
Why does nephritic syndrome decrease the glomerular filtration rate?
Because inflammation of the glomeruli leads to cell proliferation, leukocyte infiltration, and thickening of the glomerular basement membrane, which narrow or block capillary lumens, reducing the surface area available for filtration and decreasing GFR.
77
Why does a decreased glomerular filtration rate in nephritic syndrome cause hypertension, edema and oliguria?
↓ GFR causes fluid and sodium retention, activating the RAAS (the kidney responds to low GFR as if it were hypoperfused) and increasing blood volume and systemic vascular resistance. This leads to hypertension, edema from fluid and sodium retention, and oliguria due to reduced urine output from decreased filtration.
78
In nephritic syndrome, an inflammatory process triggers the release of ________ which induce glomerular damage.
cytokines
79
Why does nephritic syndrome lead to hematuria and proteinuria?
Glomerular inflammation damages the glomerular capillary walls, increasing their permeability. This allows red blood cells and proteins (mainly albumin) to pass into the urine, leading to hematuria and mild to moderate proteinuria.
80
Why does nephritic syndrome lead to azotemia?
Azotemia is a biochemical abnormality, defined as elevation, or buildup of, nitrogenous products.
Nephritic syndrome can lead to azotemia because inflammation decreases the glomerular filtration rate (GFR), reducing the kidneys’ ability to excrete nitrogenous waste products like urea and creatinine, which then accumulate in the blood.
81
What type of edema is usually seen in nephritic syndrome?
Positive Godet edema, namely periorbital (swollen eyelids) and peripheral (swelling in the arms or legs).
82
What are the main primary causes of nephrotic syndrome?
* Minimal change disease
* Focal segmental glomerulosclerosis
* Membranous nephropathy
* Glomeruloproliferative glomerulonephritis
83
What are the main secondary causes of nephrotic syndrome?
* Diabetic nephropathy
* Amyloid nephropathy (deposition of proteins with an abnormal conformation)
* Lupus nephritis
84
How does nephrotic syndrome cause hypoproteinemia and hypoalbuminemia?
Damage to the glomerular filtration barrier increases its permeability, allowing large amounts of plasma proteins—especially albumin—to be lost in the urine. This leads to hypoproteinemia and specifically hypoalbuminemia in the blood.
85
How does nephrotic syndrome lead to lipiduria?
In nephrotic syndrome, hypoalbuminemia due to proteinuria stimulates the liver to increase lipoprotein (VLDL) synthesis, causing hyperlipidemia. Some of these excess lipids spill into the urine, leading to lipiduria, often visible as fatty casts or “oval fat bodies” in the urine.
86
Why does nephrotic syndrome cause edema?
Nephrotic syndrome causes hypoalbuminemia, which lowers plasma oncotic pressure (pressure created by proteins in the blood). This causes fluid to shift from the blood vessels into the interstitial tissues, leading to edema.
87
How does the loss of different proteins in nephrotic syndrome contribute to its complications? Refer to antibodies, antithrombin III, vitamin-D binding proteins and thyroxine-binding globulin.
The loss of various proteins in nephrotic syndrome has specific consequences:
* Antibodies → ↑ susceptibility to infections
* Antithrombin III → ↑ hypercoagulability (risk of thrombosis)
* Vitamin D-binding proteins → Vitamin D deficiency (bone health issues)
* Thyroxine-binding globulin → Thyroid dysfunction (altered thyroid hormone levels)
88
What are the main clinical manifestations of nephrotic syndrome?
* Edema
* Foamy urine
* Hypertension
* Symptoms of hypocalcemia (tetany, paresthesia, spasms)
* Muehrcke lines in fingernails (multiple transverse white linear bands parallel to the lunula of the fingernail)
89
What are tubulointerstitial diseases?
Tubulointerstitial diseases are kidney diseases that affect the kidney's tubules and interstitium (including the connective tissue and medullary vasculature).
90
What causes tubulointerstitial diseases?
1) **Bacterial infection** that reaches the kidney through:
* the bloodstream (less common)
* asceding dissemination (i.e., starts at the periurethral area and goes up through the urethra, bladder, ureter and reaches the kidneys) - **urinary tract infection** (UTI).
2) **Drugs** (penicillins, sulphonamides, NSAIDs) that lead to hypersensibility reactions or nephrotoxic lesion.
91
Why are women more susceptible than men to UTIs?
* Vaginal bacterial ‘reservoir’ (fecal origin) due to closer proximity to the anus;
* Shorter urethra;
* Absence of antibacterial secretions (men have the prostatic fluid).
92
What are the four main factors that determine the progression of a UTI?
* Genetic susceptibility to bacterial adhesion;
* Bacterial species;
* Vesicoureteral reflux (backward flow of urine from the bladder into the ureters and sometimes the kidneys);
* Uretero-renal reflux (backward flow of urine from the ureters into the renal pelvis and kidneys).
93
If an UTI reaches the kidneys, it is called ________.
pyelonephritis
94
How can we differentiate a lower UTI (restricted to the urethra and bladder) from pyelonephritis (kidney infection) based on symptoms?
* Lower UTI: Local urinary symptoms (dysuria, urgency, frequency), no systemic signs (no fever or flank pain).
* Pyelonephritis: Includes systemic signs (fever, chills, flank pain) and signs of kidney involvement like cellular casts.
95
If acute pyelonephritis is not resolved, what are the possible pathological consequences in the kidney?
* **Neutrophil infiltration** into the renal interstitium and tubules (neutrophils release proteolytic enzymes and reactive oxygen species to kill pathogens, but these molecules also damage nearby renal tissue);
* **Replacement by granulation tissue** (connective tissue) during the healing phase;
* **Possible abscess formation** if necrosis and pus accumulate;
* **Fibrosis and scar tissue formation**, potentially leading to chronic kidney dysfunction.
96
What are two major causes of acute tubular necrosis?
* Ischemia (e.g. prolonged hypotension or hypoperfusion)
* Toxins from hemolysis (free hemoglobin) or rhabdomyolysis (myoglobin release)
Both cause direct tubular cell injury, leading to necrosis and loss of function.
97
What are key vascular conditions that can lead to intrinsic renal failure?
* **Hypertensive crisis** → damages small renal vessels
* **Renal vein thrombosis** → obstructs venous outflow and increases pressure
* **Vasculitis** → immune-mediated inflammation of renal vessels
98
How do vascular diseases impair kidney function?
They reduce perfusion, cause inflammation, and/or lead to vascular obstruction, which can result in ischemia and glomerular damage.
99
How can acute tubular necrosis evolve into tubulointerstitial disease?
Persistent or severe ATN can cause chronic inflammation and fibrosis of the interstitium, leading to tubulointerstitial disease with progressive loss of renal function.
100
What are the main post-renal causes of renal failure?
Intra- (collecting ducts, pelvis) or extra-renal (ureter,bladder) obstructions which, in the absence of resolution, lead to irreversible damage
with renal atrophy. Namely:
* Renal lithiasis (kidney stones)
* Neurogenic bladder
* Benign prostatic hyperplasia
101
What are some of the conditions that cause acquired obstruction in the kidneys, ultimately leading to post-renal failure?
* Benign prostatic hyperplasia
* Neoplasms (e.g., bladder, cervix or metastases)
* Intrarenal obstruction after acute tubular necrosis event
* Single kidney lithiasis (kidney stones)
* Neurogenic bladder (condition that causes loss of bladder control due to nerve damage in the brain, spinal cord, or nerves)
* Iatrogenic (ladder injury that occurs as a result of medical care, such as surgery)
102
What is Myeloma Kidney (a.k.a. "Myeloma Cast Nephropathy")?
“Myeloma kidney” is renal impairment caused by multiple myeloma (blood cancer that develops in plasma cells in the bone marrow) or similar plasma cell dyscrasias (e.g., AL amyloidosis). It leads to intrarenal obstruction from light chain casts and tubular toxicity.
103
What are the main lifestyle risk factors for the development of renal lithiasis (kidney stones)?
* High intake of animal protein
* High sodium consumption
* Low intake of chelating agents, such as: citrate, dietary fiber and alkaline foods (e.g. fruits and vegetables)
* Low water intake
104
Why does low water intake increase the risk of kidney stones?
Reduced fluid intake lowers urine volume, increasing urine concentration and promoting crystal formation.
105
What metabolic diseases are associated with renal lithiasis?
* Hypercalciuria (excess calcium in urine);
* Hyperuricosuria (excess uric acid in urine);
* Hyperoxaluria (excess oxalate in urine);
* Hypocitraturia (low levels of citrate in urine);
* Gout (inflammatory arthritis), due to high uric acid levels.
106
How does hyperparathyroidism contribute to renal lithiasis?
Hyperparathyroidism causes hypercalcemia and hypercalciuria, promoting the formation of calcium-based kidney stones (especially calcium oxalate or phosphate).
107
Why do recurrent urinary tract infections increase the risk of kidney stones?
Certain bacteria produce urease, which raises urinary pH and promotes the formation of struvite stones (magnesium ammonium phosphate).
108
Is kidney stone formation influenced by genetics?
Yes — family history increases the risk of stone formation due to inherited metabolic or structural factors affecting urine composition.
109
How does inflammatory bowel disease (IBD) increase the risk of renal lithiasi?
In inflammatory bowel disease (especially Crohn’s disease), fat malabsorption leads to increased oxalate absorption in the gut, causing hyperoxaluria and leading to the formation of calcium oxalate stones.
110
What’s the link between obesity, hypertension, and kidney stones?
Both hypertension and obesity are associated with altered calcium and uric acid metabolism, acidic urine, and increased stone risk.
111
Why is the absence of intestinal oxalate-degrading bacteria a risk factor for kidney stones?
Some bacteria degrade oxalate in the intestine. Without them, more oxalate is absorbed and excreted in urine, increasing risk for calcium oxalate stones.
112
Which medications increase the risk of kidney stones?
Lithogenic drugs promote crystal formation in the urine. Examples:
* Loop diuretics
* Topiramate
* Indinavir
* Vitamin D in excess
* Calcium supplements
113
What are the four types of renal lithiasis?
* Calcium (oxalate or phosphate) - 80%
* Struvite (magnesium ammonium phosphate) - 10%
* Uric acid - 3-10%
* Cystine - < 2%
114
What is the main cause of struvite kidney stones?
Often due to recurrent UTIs caused by urease-positive bacteria (e.g. Proteus mirabilis).
115
What causes cystine kidney stones?
Caused by cystinuria, a recessive genetic disorder, in which defective proximal reabsorption of cysteine leads to stone formation.
116
What are the main causes of calcium (oxalate or phosphate) kidney stones?
Metabolic conditions such as hypercalciuria, hyperoxaluria, and hypocitraturia.
117
Why are struvite stones more common in females?
Because women are more prone to urinary tract infections (shorter urethra and anatomical proximity between the urethra and anus) caused by urease-positive bacteria, which increase urine pH and promote struvite crystal formation.
118
Why are uric acid stones more common in males?
Men have higher rates of gout and purine-rich diets (animal protein), which lead to acidic urine and increased uric acid levels.
119
What are the classical clinical manifestations of renal lithiasis?
* Severe flank pain
* Hematuria (macro or microscopic)
* ± Fever (may or may not be present)
120
What can bilateral lithiasis or a stone in a solitary kidney cause?
* Anuria (no urine output)
* Post-renal azotemia (↑ nitrogenous waste due to obstruction)
121
Why does hematuria occur in renal lithiasis?
The kidney stones cause mechanical trauma to the urinary tract mucosa, leading to blood in the urine.
122
What is the gold standard imaging technique for diagnosing kidney stones?
Non-contrast helical **CT scan** (CT KUB)
→ High sensitivity and specificity
→ Can detect all types of stones
→ Fast and does not require contrast
123
What are the two main imaging techniques used for the diagnosis of kidney stones?
* CT
* Ecography
124
Which imaging technique can be used to detect calcium-based kidney stones, but not for uric-acid stones?
X-ray.
It detects radiopaque stones, such as **calcium-based** stones, but misses radiolucent stones, such as **uric-acid** stones.
125
What are the three main complications of renal lithiasis?
* Hydronephrosis (accumulation of urine in the kidneys due to obstruction)
* Kidney abscess or infection
* Renal failure
126
How can kidney stones lead to hydronephrosis?
A stone obstructs urine flow, increasing pressure in the urinary tract and causing dilation of the renal pelvis and calyces (hydronephrosis).
127
Why can kidney stones cause renal abscess or infection?
Obstructed urine flow provides an ideal environment for bacterial growth, leading to urinary tract infections or renal abscess formation.
128
In what cases can kidney stones cause renal insufficiency/failure?
If bilateral obstruction or obstruction in a single functioning kidney occurs, it can result in acute or chronic kidney failure due to impaired filtration.
129
What is neurogenic bladder?
It’s a bladder dysfunction caused by a **disruption in the coordination between the central and peripheral nervous systems**, affecting storage or voiding of urine (aka bladder control).
130
Name common etiologies of neurogenic bladder.
* Multiple sclerosis
* Parkinson’s disease
* Stroke (AVC)
* Diabetes mellitus (diabetic neuropathy)
* Cauda equina syndrome
* Paralytic syndromes
* Spinal trauma
131
How can diabetes mellitus cause neurogenic bladder?
Autonomic neuropathy damages the nerves controlling bladder function, leading to impaired sensation, incomplete emptying, or overflow incontinence.
132
What are the complications associated with neurogenic bladder?
* Urinary retention
* Recurrent urinary tract infections (UTIs)
* Kidney damage (hydronephrosis, reflux)
* Incontinence
133
What is Benign Prostatic Hyperplasia?
A non-cancerous enlargement of the prostate that usually begins around age 30 and can compress the urethra, affecting urination.
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Name common urinary symptoms of Benign Prostatic Hyperplasia.
* Urinary incontinence
* Increased urinary frequency (pollakiuria)
* Nocturia (nighttime urination)
* Dysuria (painful urination)
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What complications can arise from untreated Benign Prostatic Hyperplasia?
* Urinary tract infections (UTIs)
* Kidney stones (renal lithiasis)
* Urinary retention
* Acute renal failure
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How can Benign Prostatic Hyperplasia lead to acute renal failure?
Prostatic enlargement can block urine outflow, leading to urinary retention, increased pressure in the urinary tract, and eventually reduced glomerular filtration.
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What are the four phases of acute renal failure?
* Initiation Phase
* Maintenance Phase
* Diuretic (Polyuric) Phase
* Recovery Phase
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What are the manifestations of the initiation phase of acute renal failure?
The patient may feel fatigue and discomfort, as well as symptoms of an underlying cause, but **renal function still appear normal**.
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What characterizes the maintenance phase of acute renal failure?
* Oliguria (low urine output) or anuria (no urine output) lasting 1–3 weeks
* Azotemia (↑ urea and creatinine)
* Fluid retention → peripheral edema, dyspnea, orthopnea, crackles, S3
* Metabolic changes: hyperkalemia, acidosis, uremia → lethargy, asterixis (tremors)
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What are the signs of the diuretic phase of acute renal failure?
There's an increase in the urine output, up to 3 to 5 L per day, which leads to electrolyte losses (hypokalemia, hyponatremia, hypocalcemia, hypomagnesemia).
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What defines Chronic Kidney Disease (or chronic renal failure)?
Defined by a decrease in glomerular filtration rate (GFR) or persistent albuminuria for more than 3 months.
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What structural kidney changes are seen in chronic renal failure?
* Bilateral renal atrophy (reduced kidney size)
* Interstitial fibrosis
* Glomerular scarring
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How many stages of chronic renal failure are there and what are they based on?
There are 5 stages, based on GFR levels.
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What is chronic renal failure Stage 1?
* Normal or elevated GFR > 90 mL/min
* Usually with evidence of kidney damage (e.g., albuminuria)
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What is chronic renal failure Stage 2?
* GFR = 60–89 mL/min
* **Mild** decrease in kidney function
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What is chronic renal failure Stage 3A?
* GFR = 45–59 mL/min
* **Moderate** decrease in kidney function
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What is chronic renal failure Stage 3B?
* GFR = 30–44 mL/min
* **Moderate** to severe reduction in kidney function
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What is chronic renal failure Stage 4?
* GFR = 15–29 mL/min
* Severe decrease in kidney function
* Often symptomatic
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What is chronic renal failure Stage 5?
* GFR < 15 mL/min
* End-stage chronic renal failure
* Requires dialysis or kidney transplant
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What are the six main causes of chronic renal failure?
* Diabetes mellitus (diabetic nephropathy)
* Hypertension
* Recurrent UTIs
* Glomerulopathies
* Chronic nephrolithiasis (kidney stones)
* Polycystic kidney disease
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Why do chronic renal failure patients appear pale and fatigued?
Chronic renal failure **impairs the production of erythropoietin** by the kidneys, decreasing erythropoiesis (production of red blood cells). Therefore, the portion of red blood cells in the blood decreases (low hematocrit), leading to **anemia**, which causes fatigue and paleness. Additionally, chronic renal failure may cause **GI hemorrhage** due to uremic platelet dysfunction (caused by the accumulation of uremic toxins), which further worsens the anemia and contributes to fatigue and paleness.
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Why does uremia cause medullary suppression in chronic renal failure?
Uremia is a buildup of waste products in the blood. It causes medullary suppression in chronic renal failure due to **toxic effects of uremic toxins on the bone marrow**.
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What are the possible sodium imbalances in chronic renal failure?
Hyponatremia or Hypernatremia, due to impaired sodium regulation by the kidneys.
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Why does chronic renal failure often lead to hyperkalemia?
Due to decreased renal potassium excretion, as the kidneys are less able to filter and excrete potassium properly.
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Why does chronic renal failure cause metabolic acidosis?
The kidneys' reduced ability to excrete hydrogen ions (H⁺) and reabsorb bicarbonate (HCO₃⁻) results in an accumulation of acids in the body.
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Why does chronic renal failure lead to osteodystrophy?
Chronic renal failure leads to **decreased active vitamin D production** due to impaired kidney function. This causes **hypocalcemia**, which triggers secondary hyperparathyroidism (high PTH levels). The increased PTH causes bone resorption, while the lack of vitamin D impairs bone mineralization, leading to **osteodystrophy** (bone abnormalities).
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How does uremia lead to immune suppression in chronic renal failure?
Uremia (accumulation of waste products in the blood) causes leukocyte suppression due to uremic toxins, particularly affecting lymphocytes. This suppression leads to impaired immune response, making the body more susceptible to infections and diseases.
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How does chronic renal failure affect pregnancy and fertility?
Chronic renal failure (CRF) can disrupt hormonal regulation due to decreased glomerular filtration rate (GFR), leading to:
* Pregnancy: Reduced GFR increases prolactin, endorphins, and leptin levels, which suppress GnRH (gonadotropin-releasing hormone) production. This suppression results in **reduced estrogen levels**, causing amenorrhea (absence of menstruation) and increasing the risk of pregnancy interruption.
* Fertility: Similar hormonal changes (e.g., increased prolactin and reduced GnRH) lead to **decreased testosterone levels**, causing impotence and oligospermia (low sperm count), which can result in sexual dysfunction and infertility.
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Why does diabetes mellitus often stabilizes or appears to improve in chronic renal failure?
Chronic renal failure results in reduced renal degradation of insulin. This leads to higher plasma insulin levels. As a result, insulin’s effectiveness in controlling blood sugar increases, which may stabilize diabetes mellitus.
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What are the cardiovascular manifestations of chronic renal failure?
* Uremic pericarditis (due to uremia)
* Congestive heart failure and/or pulmonary edema (due to blood volume overload)
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What central nervous system symptoms can occur in chronic renal failure?
* Sleep disturbances
* Difficulty concentrating
* Memory loss
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What are the peripheral nervous system-related symptoms in chronic renal failure?
* Neuromuscular irritability
* Peripheral neuropathy
* Asterixis, myoclonus, seizures, coma (in advanced uremia)
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What gastrointestinal symptoms are seen in chronic renal failure?
* Peptic ulcers (due to secondary hyperparathyroidism)
* Nausea and vomiting
* Gastroenteritis
* Anorexia
* Diverticulitis
* Uremic fetor (urine-like breath odor)
* Hiccups
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What skin symptoms are associated with chronic renal failure?
* Pallor/paleness (due to anemia)
* Hyperpigmentation
* Easy bruising (ecchymosis)
* Transfusion-induced hemochromatosis (excess iron absorption)
* Pruritus (calcium/phosphate deposition)
* Uremic frost (crystallized urea on skin)
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What are the two main types of dialysis?
* **Hemodialysis**: Uses a machine to filter blood outside the body.
* **Peritoneal dialysis**: Uses the body's natural lining to filter blood inside the body (permanent access).
