Term
| What type of cast would you see with proteinuria? |
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Definition
| Hyaline casts are often present with proteinuria. They look clear and "proteinaceous" :P |
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Term
| What type of cast would you see in nephritic syndrome? |
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Definition
RBC casts are observed with nephritic syndrome. They are brownish in color.
Glomerulonephritis results in inflammatory rupture of glomerular capillaries, which leads to bleeding into Bowman's space. |
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Term
| What type of cast would you see in acute pyelonephritis? |
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Definition
As it is an infection process in the kidneys, pyelonephritis results in WBC casts in the urine. These are composed mainly of neutrophils and eosinophils.
Pyelonephritis also presents with granular casts, from cell death and breakdown. |
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Term
| What type of cast would you see in nephrotic syndrome? |
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Definition
| Fatty casts/ the "maltese cross" can be seen in nephrotic syndrome. |
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Term
| What type of cast would you in Acute Tubular Necrosis? |
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Definition
| Epithelial casts and granular casts, created by the breakdown of tubular epithelial cells, are observed in ATN. |
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Term
| Waxy casts are seen in what type of renal disease? |
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Definition
| Waxy casts are present in Chronic Renal Failure. |
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Term
| If there is an equivalent increase in BUN and Creatinine, are you dealing with pre-renal, renal, or post-renal azotemia? |
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Definition
| Renal. BUN is reabsorbed in the kidney, while creatinine is not(for the most part). Therefore, in pre-renal, GFR decreases, slowing movement through the tubules and allowing more time for reabsorption of solutes (i.e. BUN but not much creatinine). Therefore BUN will increase more. In post-renal, the back-up of urine and the resulting increase in pressure pushes BUN back through the tubular epithelium, favoring its reabsorption to an even greater degree. This will show the greatest BUN/Cr increase of the 3 types of azotemia. If the problem is renal, then there is likely a problem with filtration, so both BUN and creatinine will rise together, being affected before the tubular reabsorption can preferentially cause an increase of just BUN. |
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Term
| How can kidneys be related to Fibrinous Pericarditis? |
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Definition
| Uremia is a risk factor for fibrinous pericarditis |
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Term
| A patient is found to have an abdominal mass. On imaging a unilaterally enlarged, multicystic kidney is observed. Microscopic examination reveals undifferentiated mesenchyme. You diagnose it as the most common congenital renal abnormality. What is your diagnosis? |
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Definition
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Term
| Describe the features of autosomal dominant polycystic kidney disease |
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Definition
ADPKD is due to a mutation in PKD1 (85%) or PKD2 (15%) and results in bilaterally enlarged kidneys, Symptoms don't begin until roughly the 4th decade. Eventually all the renal parenchyma is replaced by 3-4cm cysts and 40% of these patients progress to renal failure within 10 years of diagnosis.
Association with berry aneurysms, a potentially fatal complication!
(as well as hepatic/splenic cysts and diverticulosis) |
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Term
| What would you see in autosomal recessive polycystic kidney disease? |
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Definition
| autosomal recessive polycystic kidney disease presents as renal failure at birth! (vs. autosomal dominant) The kidneys are bilaterally affected, contain many small cysts. Cysts may also be found in the liver. |
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Term
| Why does nephrotic syndrome lead to hyperlipidemia? |
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Definition
| Recall that in nephrotic syndrome there is massive protein loss i the urine (>3.5g/day). Hyperlipidemia results from a compensatory increase in lipoprotein synthesis to try to maintain blood protein levels. |
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Term
| In which condition would you find linear deposition of antibody in the glomeruli? |
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Definition
| Goodpasture's Syndrome, in which there are anti-GBM antibodies, will show smooth, linear deposition. Recall that Goodpasture's affects the lung and kidney. These two systems will be affected in the patient's presentation. |
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Term
| Which conditions show a "lumpy-bumpy" immune deposition in the renal glomeruli? |
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Definition
Post-Streptococcal GN and SLE result in immune complex deposition in the glomerular basemement membrane. This does not have the smooth, linear pattern seen in Goodpastures with the anti-GBM antibodies.
Specifically, Post-Steptococcal GN has subepithelial deposits and SLE has subendothelial deposits. |
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Term
| What are changes seen in diabetic nephropathy? |
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Definition
Podocyte detachment/apoptosis, GBM thickening, Mesangial Cell hypertrophy, increased mesangial ECM.
(way to remember: diabetes= increased suger, makes glomerular basement membrane structures fat! (increased ECM, GBM thickness, hypertrophy) Podo sounds like pogo stick... fat people break pogo sticks, so podocytes apoptose... haha awful) |
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Term
| What is the most common cause of nephrotic syndrome in children? |
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Definition
Minimal Change Disease
This is a sudden onset of proteinuria (>3.5g/day) but the BP, GFR etc. are all normal. Pathological changes are not readily apparent.
Minimal Change Disease has a good prognosis. |
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Term
| An african american HIV patient and known heroin addict presents hypertension and reduced urine output. He has hematuria. Microscopic examination of his kidneys demonstrates podocyte loss, increased ECM, C3 and IgM trapping, and interstitial fibrosis. What is your diagnosis? |
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Definition
Focal Segmental Glomerulonephritis
This is associated with a poor prognosis, especially in HIV/IV drug abusers, where it is more likely to lead to rapidly progressing cases. |
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Term
| The "wire-loop" appearance and silver stain spike formation can be observed in what form of glomerulonephritis? |
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Definition
Membranous Glomerulonephritis/Glomerulopathy
This is immune complex mediated. Antibody complex deposition in the GBM activates the complement system. The mesangium is not affected in Membranous GN, whereas the mesangium is affected in membranoproliferative GN.
The silver spikes are formed by the granular IgG immune complexes.
This can be due to SLE, Malignancies, Hepatitis, or most commonly: Idiopathic! |
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Term
| Which glomerulonephritis shows a double GBM (railroad track appearance)? |
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Definition
| A "railroad track" GBM can be seen in Membranoproliferative GN, (specifically Type I). Cellular interpositions split the GBM, creating a double-layered appearance. |
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Term
| What do you know about Post-Streptococcal glomerulonephritis? |
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Definition
| 6-14 days after a B-hemolytic Strep infection (ex: strep throat), granular immune complex deposition on the subepithelial GBM leads to complement activation and an inflammatory reaction. This can be visualized as hypercellular glomeruli with neutrophils. On the external surface of the kidney, there will be a "flea-bitten" appearance. |
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Term
| What are the features of IgA nephropathy? |
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Definition
IgA nephropathy, which is a component of Henoch-Schonlein Purpura, often involves proteinuria, hematuria, and usually follows an illness (ex: upper respiratory viral infection).
IgA deposits in the mesangium, leading to a mesangial immunofluoresence pattern. Mesangial hypercellularity and increased ECm are also present. |
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Term
| What disease has remodeling of the GBM into a basket-weave pattern, nesangial hypercellularity, but no Ig deposition? |
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Definition
Alport's Syndrome.
This disease presents with endstage renal disease and nerve deafness. Ocular disorders may also be present. Hematuria and proteinuria are always present!
This involves mesangial hypercellularity, like IgA nephropathy... but there is no Ig deposition in Alport's Disease, unlike IgA Nephropathy.
Alport's Syndrome is found in patients with mutations of collagen genes. (most commonly X-linked, but may also be autosomal recessive). When mutations prevent the formation of type IV collagen fibers, the basement membranes of the kidneys are not able to filter waste products from the blood and create urine normally, allowing blood and protein into the urine. The abnormalities of type IV collagen in kidney basement membranes cause gradual scarring of the kidneys, eventually leading to kidney failure in many people with the disease. Progression of the disease leads to basement membrane thickening and gives a "basket-weave" appearance from splitting of the lamina densa. |
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Term
| What are the three types of rapidly progressive glomerulonephritis? |
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Definition
Rapidly progressive glomerulonephritis is also called "crescentic glomerulonephritis". Here, there is rapid progression to renal failure in weeks to months.
Type I = Anti-GBM (goodpastures)
Type II = Immune Complex Mediated
(Post-Streptococcal, SLE, IgA Nephropathy)
Type III = Pauci-Immune/ ANCA-associated
(Wegener's, Polyarteritis Nodosa; i.e. vasculitides)
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Term
| What are the classes of lupus nephritis? |
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Definition
Lupus nephritis has 5 classes (sometimes 6 are stated)
1) Minimal Mesangial
2) Mesangial Proliferative
3) Focal Proliferative
4) Diffuse Proliferative
5) Membranous |
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Term
| decreased GFR, increased creatinine, and Granular (dirty brown) & Epithelial casts should point you toward what renal condition? |
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Definition
| These should signify acute tubular necrosis (ATN), a potentially reversible acute renal failure. It is the most frequent cause of acute renal failure. |
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Term
| List some causes of Acute Tubular Necrosis |
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Definition
Renal Hypoperfusion (hypovolemic shock, septic shock, malignant hypertension)
Toxins (Aminoglycosides, contrast dye, ethylene glycol) |
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Term
| Which disease demonstrates a linear immunofluorescence pattern and crescentic glomerulonephritis? |
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Definition
| Goodpasture Syndrome, which may also present with hemoptysis because the anti-GBM antibodies also attack the pulmonary BM. |
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