Pathologie der Nieren

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Adrenal haemorrhage / Waterhouse-Friderichsen Syndrome
Clinical HistoryA 77-year old male presented with a 3-day history of abdominal and flank pain with fevers and rigors. He was 2 weeks post-operative from a duodenal ulcer repair surgery. He was hypotensive, hyperkalemic and hyponatremic with a purpuric rash. His blood cultures grew Escherichia coli. He failed to respond to treatment, and died soon after admission due to septic shock.PathologyThe combined kidney and adrenal gland have been mounted, in order to display the cut surfaces. Extensive haemorrhage has occurred into the adrenal medulla, and there is some extravasation of blood into the periadrenal fat. This is an example of adrenal haemorrhage in the setting of severe septic shock also known as ‘Waterhouse-Friderichsen’ syndrome.Further Information Waterhouse-Friderichsen syndrome is characterised by adrenal haemorrhage cause by overwhelming sepsis leading to hypotensive shock, disseminated intravascular coagulation (DIC) and adrenocortical insufficiency. It most commonly occurs in children and rarely in adults. Neisseria meningitis causes over 80% of cases of adrenal haemorrhage. Other organisms that may cause it include Streptococcus pneumoniae, pseudomonas aeruginosa, Escherichia coli, Klebsiella pneumoniae, Haemophilus influenzae and staphylococci.The exact cause of the haemorrhage is unclear. It may be due to bacterial seeding of the adrenal vessels, to the DIC or to endothelial dysfunction from inflammatory mediators or bacterial toxins. Adrenal haemorrhages can occur bilaterally. The haemorrhage begins in the medulla and extends outwards to the cortex, and may extend into the periadrenal fat. This leads to adrenal gland failure. Patients present with rapidly progressive septic shock, diffuse purpuric skin rash and adrenal insufficiency crisis. Treatment includes supportive therapy, intravenous antibiotics directed against the cultured organisms, and steroid therapy. The mortality rate is over 50%.

386,75 €*
Adult polycystic kidney disease
Clinical HistoryA 40-year old male attends his GP complaining of 2 weeks of haematuria and new onset of headache with blurred vision. His GP notes a blood pressure of 260/110 and refers the patient to hospital. The patient collapses on arrival to hospital. A CT brain shows a large subarachnoid haemorrhage from a ruptured ‘berry’ aneurysm. The patient dies shortly after admission.PathologyThe specimen is an enlarged kidney. The renal parenchyma has been almost completely replaced by numerous dilated cysts varying in size, up to 3cm in diameter. The cysts have thin translucent walls, and some cysts contain material of varying colours, giving a ‘marble-like’ appearance to the cut surface of the kidney. The varying colours are caused by the secretions within the cysts, which may be admixed with haemorrhage. The external surface appears lobulated as a result of multiple projecting cysts. Any remaining renal parenchyma is severely atrophic caused by the pressure of the numerous cysts. This is an example of adult polycystic kidney disease.Further InformationAdult polycystic kidney disease (APKD) is an autosomal dominant disorder characterised by the presence of multiple cysts within the renal parenchyma. The cysts develop from altered renal tubule epithelium. The cysts expand destroying the glomeruli, causing ischaemia, pressure atrophy, and eventually leading to renal failure.APKD occurs in 1 in 40 to 1000 live births. Mutations in the PKD1 gene on chromosome 16p13.3 and PKD2 gene on chromosome 4q21 have been described as causal mutations. These code for membrane proteins polycystin 1 and 2, respectively. Patients with PKD1 mutation are more common and have a more severe phenotype. End stage renal disease (ESRD) occurs at a mean age of 74.0 in PKD2 versus 54.3 years in PKD1.Common symptoms of APKD include haematuria from haemorrhage into cysts and pain or a sensation of dragging from the expansion of cysts and kidney enlargement. Many patients remain asymptomatic until features of renal failure occur such as proteinuria, polyuria, hypertension and uraemia. Extrarenal manifestations of the disease include intracranial ‘berry’ aneurysms, hepatic and pancreatic cysts, as well as mitral valve prolapse and other types of cardiac valve disease. Renal ultrasound is the most common investigation used to diagnose APKD. CT- and MRI scans may also be used as diagnostic tools. Patients with a positive family history of APKD can be offered screening renal US scans and genetic testing in some cases. Treatment involves renal replacement therapy for ESRD and renal transplant (if a donor can be found).Ultimately, over one-third of patients die from renal failure and one-third from coronary or hypertensive heart disease. Approximately 1% of patients die from subarachnoid haemorrhage, because of berry aneurysm rupture (as in this case). Remaining deaths are due to unrelated causes.

535,50 €*
Hydronephrosis Hydroureter
Clinical HistoryA 49-year old male presents with a 6-week history of malaise, urinary frequency and haematuria for 6 weeks. Further questioning revealed intermittent left flank pain. Abdominal ultrasound showed severe hydronephrosis and hydroureter, secondary to multiple obstructing ureteric calculi at the uretero-vesical junction. He underwent a left nephrectomy and ureterectomy, and made a successful recovery.PathologyThis is the patient’s left nephrectomy and ureterectomy specimen. The kidney has been bisected and the cut surface of both halves is displayed, mounted in continuity with the ureter, which has been opened. The kidney is grossly hydronephrotic, and there is considerable atrophic thinning and loss of renal parenchymal tissue. The ureter is extremely dilated and distally contains a number of small brown-black calculi with irregular sharp surface projections. These are calcium oxalate stones.This is an example of hydronephrosis and hydroureter due to calculi obstructing the lower end of the ureter.Further InformationHydronephrosis, or obstructive uropathy, is the dilation of the renal pelvis and calyces caused by an obstruction in the urine outflow. Obstruction can occur at any point in the urinary tract. Any lesion-, intrinsic (within the outflow system) or extrinsic (outwith the ureter)-, that impedes the flow of urine can lead to hydronephrosis. Common causes include: congenital anomalies, urinary calculi, urinary tract tumours, urinary tract inflammation, prostatic hypertrophy, and prostate tumours. Symptoms of the hydronephrosis relate to the pathology causing the obstruction (e.g. renal colic pain with calculi), the time period of the obstruction (acute or chronic), the site (unilateral or bilateral) and whether it is complete or partial.If the obstruction is not relieved it will ultimately cause pressure to build up proximal to the obstruction. This pressure is transmitted in a retrograde manner through the collecting ducts to the cortex causing progressive atrophy of the kidney with dilatation of the renal calyces and pelvis. The pressure also compresses the vasculature in the medulla leading to ischaemic medullary damage. Glomerular filtration persists in the affected kidney until late in the disease process when the filtration gradually diminishes or ceases. Obstruction triggers an interstitial inflammatory process leading to fibrosis. Ultrasound is the key diagnostic tool for diagnosis followed by CT or urogram. Most obstructing lesions require surgical intervention to relieve the blockage. Surgical interventions depend on each individual cause, but include nephrostomy or stenting for upper urinary tract obstruction and urinary catheter or suprapubic catheter insertions for lower urinary tract obstructions.

697,34 €*
Horseshoe Kidney
Clinical HistoryThis specimen was found during a routine post-mortem of a 56-year-old male who died of rheumatic heart disease.PathologyThe kidney is 12 cm in length and the two parts are fused at the lower pole forming this horseshoe-like shape. The ureters can be seen emerging from the hilum on the anterior aspect of the 3D print. The kidney is bisected in the horizontal plane which is evident on the posterior aspect. There is persistent foetal lobulation. The renal pelvis is characteristically antero-medial positioned with the ureters travelling anterior to the fused lower poles or isthmus of the kidney.Further InformationHorseshoe kidneys are the commonest renal developmental abnormality. This anomaly is twice as common in males as in females. They are found in about 1 in 500 to 1000 post-mortem examinations. Most cases are sporadic but may be associated with some chromosomal anomalies, such as those resulting in Downs and Edwards Syndromes as well as non-aneuploidic anomalies, such as VACTERL* association. In 90% of cases an isthmus of renal tissue connects the lower poles of the kidneys across the midline, forming a horseshoe shape. Fusion of the upper lobes is rare. The renal pelves that drain the two halves of the horseshoe kidney are directed more anteriorly than normal and there is some angulation of ureters as they cross the isthmus.This malformation is usually asymptomatic and picked up incidentally on routine ultrasound or CT scans. These kidneys usually function normally. There is an increased incidence of urinary calculi, possibly due to angulation of the ureters and to the resulting stasis. There is an increased risk of hydronephrosis usually from pelvi-ureteric junction obstruction. There is a higher incidence of urinary tract infections mainly due to vesico-ureteric reflux. A higher incidence in some forms of renal malignancies (e.g. transitional cell carcinoma and Wilms tumours) has also been described.(*VACTERL = Vertebral defects, Anal atresia, Cardiac defects, Tracheo-Esophageal fistula, Renal anomalies, and Limb abnormalities).

596,19 €*
Septic Renal Infarct
Clinical HistoryA 54 year old male patient presents with flank pain. He is an active intravenous drug user. Further questioning reveals a history of intermittent haematuria, fevers, malaise and vomiting. On examination he is hypertensive and pyrexic. Inspection of his limbs reveals Janeway lesions on his extremities and track marks from recent IV drug use. A systolic murmur is found on auscultation of his chest. Blood tests reveal elevated inflammatory markers, impaired renal function, elevated LDH and multiple bacteraemic blood cultures. Echocardiogram shows a large mobile tricuspid vegetation. He was commenced on treatment for infective endocarditis but later died from a sudden cardiac arrest.PathologyThe specimen is the patient’s kidney from post mortem examination. The kidney has been bisected with a cut half surface on display. There are multiple well demarcated wedge shaped pale yellow-white areas evident within the cortex. The base of these pyramids lies against the cortical surface and extend along the renal columns with the apex pointing toward the medulla. The largest is evident lateral upper pole of the kidney. Theses pale areas are infarcted renal tissue. There are dark irregular shaped areas which represent areas of hemorrhage.Further InformationRenal infarction results from an interruption in the blood flow to the kidney. The kidneys receive almost a quarter of the cardiac output but have limited collateral circulation. The cortex is the most susceptible area to infarction given blood supply is from proximal to distal. The main causes of interruption of this circulation are cardioembolic disease, renal artery damage, hypercoagulable states or idiopathic.Cardioembolic causes are the most common. These include post-myocardial infarction mural thrombi, septic emboli from infective endocarditis and emboli from mechanical valves. Idiopathic renal infarction is the second most common cause. Damage to the renal artery is the third most frequent cause and includes renal artery dissection, acute vasculitis of polyarteritis nodosa, trauma or post endovascular intervention. Hypercoagulable states are the rarest cause of renal infarcts such as hereditary thrombophilia and antiphospholipid syndrome. Infarction is bilateral in ~15% of cases.Presentation of renal infarction depends on the underlying etiology. It can be clinically silent. Common manifestations include costovertebral angle pain, haematuria, hypertension due to increased renin release, nausea, vomiting and sometimes fever.Laboratory test used to aid diagnosis include urinalysis for hematuria and serum creatinine levels which may be elevated, especially in bilateral disease. CT abdomen with contrast is the first choice radiological investigation. A wedge-shaped perfusion defect is the classic finding. Treatment varies depending on the cause of the infarction but generally involves supportive therapy and treatment of the underlying pathology.

205,87 €*
Renal Cell Carcinoma
Clinical HistoryA 64-year old male presents with a 5-month history of generalised malaise, weight loss and dull right flank pain. On examination, there is a palpable right sided abdominal mass. He is noted to be hypertensive. Urinalysis reveals microscopic haematuria. The patient underwent right nephrectomy.PathologyThe specimen is a kidney, which has been incompletely dissected in the coronal plane, and mounted to display the cut surface. The lower pole of the kidney has been replaced by a rounded ill-defined irregular mass 5cm in diameter, which has compressed and distorted the overlying renal parenchyma. The cut surface of the tumour has a variegated appearance caused by areas of haemorrhage and necrosis. Several small pale-yellow tumour nodules are present in the cortex and medulla above and separate from the lower pole tumour. These are intrarenal metastases. The renal pelvis appears slightly dilated with some blunting of the renal papillae, suggesting a degree of hydronephrosis. The capsular surface is finely nodular with a few coarse scars and contains several small simple cysts (see rear of specimen). Histologically, the tumour was diagnosed as a renal cell carcinoma.Further InformationRenal cell carcinoma (RCC) comprise 85% of the primary renal malignancies. They originate within the renal cortex. The risk of developing RCC is doubled in males. It most commonly occurs in the 6th decade of life. Other risk factors for RCC include smoking, obesity, hypertension, unopposed estrogen therapy, as well as exposure to asbestos, petroleum and heavy metals. Most RCC are sporadic but around 5% are due to autosomal dominant familial cancers, such as Von Hippel Lindau syndrome, hereditary leiomyomatosis and Birt-Hogg-Dubé syndrome.There are several major primary renal tumour types according to genetic and histological tumour characteristics: clear cell carcinoma (70-80%), papillary carcinoma (10-15%), chromophobe carcinoma (5-10%), oncytic carcinoma (3-7%) and collecting (Bellini) Duct carcinoma (<1%).Clear cell carcinoma typically have a deletion of chromosome 3p and arise from the proximal tubule. They may be solid or less commonly cystic. They occur in association with Von Hippel Lindau as well as sporadically. Papillary carcinomas arise from the proximal tubule. They are associated with trisomies 7 and 17; loss of Y in male patients; and MET kinase domain mutations. They are frequently multifocal in origin. Chromophobe carcinoma originate from intercalated cells of the collecting ducts. They are associated with multiple chromosome losses and hypodiploidy. They have a low risk of disease progression.Renal oncocytic carcinomas are typically comprised of well-differentiated cells with prominently eosinophilic granular cytoplasm; they are associated with a good prognosis. In contrast, collecting (Bellini) duct carcinoma of the kidney is a highly aggressive tumour with an extremely poor prognosis as it does not respond well to chemotherapy drugs used for renal cell carcinoma, and progresses and spreads more quickly. It is a variety of renal cell carcinoma (RCC) arising from the distal segment of the collecting ducts of Bellini in the renal medulla.The typical clinical features of RCC are costovertebral pain, palpable mass and haematuria. RCC is the great mimic in medicine producing many manifestations including: polycythemia, hypercalcaemia, hypertension, pyrexia, Cushing‘s syndrome, eosinophilia and amyloidosis. RCC tend to metastasize before producing may local symptoms. The most common sites of distal spread are the lungs (50%) and bones (33%) followed by lymph nodes, adrenal glands and brain. RCC has a tendency to invadethe renal vein and extend up it as a tumour thrombus, growing as a solid column extending upto the inferior vena cava.Ultrasound and CT are the most common investigations used to assess renal lesions and diagnose RCC. A tissue biopsy may be required in some patients. An increasing number of patients are being diagnosed with RCC because of incidental kidney lesions being detected on abdominal CT requested for other medical reasons.The average 5-year survival rate for RCC is 70%. Treatment depends on the stage of the tumour. Radical nephrectomy is the usual surgical option. Medical treatment includes chemotherapeutic drugs as well as Vascular endothelial growth factor (VEGF) inhibitors and tyrosine kinases inhibitors in patients with metastatic disease.

510,51 €*
Papillary Transitional Cell Carcinoma of the Renal Pelvis
Clinical HistoryA 60 year old man who had worked in a paint factory for 40 years developed painless haematuria for one month. CT scan showed a suspected tumour in the left renal pelvis. He underwent a nephrectomy.PathologyThis is the post-nephrectomy kidney. Of note the kidney maintains its foetal lobulation. There is a friable papillary tumour of 35mm in diameter projecting in the renal pelvis. The renal pelvis is visibly dilated due to this obstructing tumor. Histological examination revealed this is papillary transitional cell carcinoma arising in the renal pelvis.Further InformationBetween 5-10% of primary renal cancers arise in the urothelium lining the renal pelvis and calyces. These are similar to tumours which may arise in the ureter and urinary bladder. These tumours range from benign papillomas (rare) to well differentiated papillary carcinomas , which are common, and poorly differentiated tumours which can be either papillary, or flat and infiltrating.Symptoms of these renal pelvis tumors tend to occur early. Due to the friable nature of the tumours haematuria is common. As they tumours grow obstructive symptoms such as palpable hydronephrosis and flank pain can be noticed. The tumours can sometimes be multiple; involving the pelvis, ureter and bladder.There is an increased risk in developing urothelial tumours in individuals with Lynch syndrome and analgesic nephropathy. Smoking significantly increases the risk of developing urothelial tumours. Industrial chemicals called aromatic amines, such as benzidine and beta-naphthylamine, which are sometimes used in the dye industry, can lead to urothelial cancers.Infiltration of the wall of the pelvis and calyces is common in theses tumour. The prognosis with infiltration is not good. 5 year survival rates vary from 50-100% for low grade and non-invasive lesions to 10% for high grade infiltrating tumours.

572,39 €*
Multiple Renal Calculi
Clinical HistoryA 68-year old male presented with fevers and rigors. Further questioning reveals a 6-month history of intermittent bilateral flank pain and haematuria. Biochemical investigations reveal significantly impaired renal function with a normal serum calcium. A CT abdomen showed bilateral hydronephrosis with multiple renal calculi as well as perinephric and subphrenic abscesses. He later died from progressive renal failure.PathologyThe specimen is patient’s kidney, which is grossly and partially bisected. There is gross dilatation of the pelvi-calyceal system visible. Significant atrophy of renal tissue can be seen, in some places being reduced to a mere rim. A large mottled brown-white calculus lies in the pelvis, and a smaller calculus occludes the ureter lumen. The ureter is dilated proximal to the impacted calculus. There are multiple calculi visible within the calyces of the specimen.Further InformationUrolithiasis (renal calculi) is a very common disease affecting up to 1 in 10 individuals during their lifetime. Formation of the stones can occur anywhere along the urinary tract but most commonly occurs within the kidneys. Risk factors for stone formation include male gender; any condition that affects the composition of the urine, such as hypercalciuria or high urine oxalate; systemic metabolic disorders, such as cystinuria and gout; dietary factors, such as high oxalate and animal protein intake, low fluid intake; and environmental factors, such as high dry temperatures. 80% of renal calculi are unilateral.Symptoms of urolithiasis include excruciating pain, haematuria, nausea, vomiting, fainting, dysuria and urgency. Symptoms depend on the size and the site of the calculus. Urolithiasis can be asymptomatic especially if the stones are formed and remain within the renal pelvis or bladder. Symptoms occur when the stones move into the ureter. Pain from calculi is usually colicky and typically severe in nature; occurring in paroxysms. The flank is the most common site for pain but pain can occur anywhere along the urinary tract and into the genitals. Pain resolves on passage of the stone. Haematuria can be gross or microscopic.There are four main types of renal calculi:Calcium stones are the most common, comprising 70% of all stones. They are made up of calcium oxalate or a mixture with calcium phosphate. Hypercalciuria, hypercalcemia and hyperoxaluria are common causes of these stones.Struvite stones make up 5-10% of stones. They are comprised of magnesium ammonium phosphate. These are commonly formed as a result of proteus infections and lead to the formation of very large “staghorn” calculi.Uric acid stones make up 5-10% of calculi. These occur in patients with hyperuricemia, such as gout and chronic leukaemias.The remainder are made up of cysteine, which is due to impaired renal reabsorption of amino acids such as cystine.Diagnosis can be made based on the medical history and examination. Radiological tools frequently used to assist diagnosis include non-contrast CT or ultrasound of the kidneys and bladder. Less commonly used imaging methods include abdominal X-ray, intravenous pyelogram and magnetic resonance imaging.If left untreated renal damage and failure from progressive obstruction. Renal calculi also predispose patients to infection secondary to obstruction and trauma that they cause. Treatment in acute patients include supportive treatment to allow the passage of the stone. Medical treatment used includes analgesia, commonly NSAIDs and opiates, and agents to aid passage of the stone, such as alpha blockers, calcium channel blockers and antispasmodics. Surgical intervention may be required if there are severe complications due to calculi or if the stone is large and unable to be expelled with conservative treatment. Surgical interventions include lithotripsy (using lasers or electricity), laparoscopic stone removal or percutaneous stone removal. Open surgery is rarely required.

489,09 €*
Hydronephrosis and Hydroureter Caused by Obstruction by a Renal Calculus
Clinical HistoryA 72-year old female presented with colicky flank pain and increasing malaise. Intermittent haematuria was noted. Biochemical investigations reveal significantly impaired renal function. CT abdomen showed congenital renal agenesis of the left kidney and a right-sided hydronephrosis and hydroureter, due to obstruction by a smaller calculus. Percutaneous lithotomy was attempted to relieve the obstruction, but the patient died of a cardiac event during the procedure.PathologyThe specimen is patient‘s right kidney, which is grossly and partially bisected. There is gross dilatation of the pelvi-calyceal system visible and significant atrophy of renal tissue particularly in the cortex. There is a large brown calculus visible in the renal pelvis at the ureteropelvic junction.Further InformationUrolithiasis (renal calculi) is a very common disease affecting up to 1 in 10 individuals during their lifetime. Formation of the stones can occur anywhere along the urinary tract but most commonly occurs within the kidneys. Risk factors for stone formation include male gender; any condition that affects the composition of the urine, such as hypercalciuria or high urine oxalate; systemic metabolic disorders, such as cystinuria and gout; dietary factors, such as high oxalate and animal protein intake, low fluid intake; and environmental factors, such as high dry temperatures. 80% of renal calculi are unilateral.Symptoms of urolithiasis include excruciating pain, haematuria, nausea, vomiting, fainting, dysuria and urgency. Symptoms depend on the size and the site of the calculus. Urolithiasis can be asymptomatic especially if the stones are formed and remain within the renal pelvis or bladder. Symptoms occur when the stones move into the ureter. Pain from calculi is usually colicky and typically severe in nature; occurring in paroxysms. The flank is the most common site for pain but pain can occur anywhere along the urinary tract and into the genitals. Pain resolves on passage of the stone. Haematuria can be gross or microscopic.Diagnosis can be made based on the medical history and examination. Radiological tools frequently used to assist diagnosis include non-contrast CT or ultrasound of the kidneys and bladder. Less commonly used imaging methods include abdominal X-ray, intravenous pyelogram and magnetic resonance imaging.If left untreated renal damage and ultimately renal failure from progressive obstruction and hydronephrosis will occur. If the obstructing calculus is not relieved it will cause pressure to build up proximal to the obstruction. This pressure is transmitted back through the collecting ducts to the cortex causing progressive atrophy of the renal parenchyma with dilatation of the renal calyces and pelvis. The pressure also compresses vasculature in the medulla leading to ischaemic medullary damage. Glomerular filtration persists in the affected kidney until late in the disease process when it will gradually diminish. Obstruction triggers an interstitial inflammatory process leading to fibrosis. Renal calculi also predispose patients to infection secondary to obstruction and the trauma that they cause to the urothelium.Treatment in acute patients include supportive treatment to allow the passage of the stone. Medical treatment used includes analgesia, commonly NSAIDs and opiates, and agents to aid passage of the stone, such as alpha blockers, calcium channel blockers and antispasmodics. Surgical intervention maybe required if there are severe complications due to calculi or if the stone is large and unable to be expelled with conservative treatment. Surgical interventions include lithotripsy (using lasers or electricity), laparoscopic stone removal or percutaneous stone removal. Open surgery is rarely required.

684,25 €*
Pyonephrosis
Clinical HistoryA 38-year old female presents with severe nausea, vomiting, fevers and rigors. She has a history of recurrent urinary tract infection over the past 6 months. She has required several courses of oral antibiotics, and one admission for IV antibiotics. Blood tests show raised inflammatory markers. Urinalysis is positive for white blood cells (WBC). A CT scan shows unilateral left hydronephrosis and pyelonephritis. She fails to respond to conservative treatment, and undergoes a nephrectomy. She makes a complete recovery.PathologyThis is the patient’s left nephrectomy specimen. The kidney has been sliced to display the cut surface. The pelvis and calyces are greatly dilated, and contain remnants of yellow pus. There is considerable fibrosis of the renal parenchyma. In the mid-zone near the lateral border, there is a hemorrhagic necrotic area 35 x 12 mm in diameter containing pus. There are two similar small hemorrhagic necrotic areas visible on the capsular surface. These lesions are probably continuous with the lesion seen on the cut surface, likely to be caused by haemorrhage into an abscess cavity. This lesion would have resulted in a perinephric abscess.Further InformationPyonephrosis occurs when there is an obstruction within the upper urinary tract and pyelonephritis. Debris of infection, WBC and bacteria collect in the obstructed kidney, resulting in a hydronephrotic kidney that is filled with pus. A staghorn calculus usually forms in association with chronic or recurrent infection as a consequence of the more alkaline urinary pH caused by the bacterial infection.Pyonephrosis is a rare condition. Risk factors for development include immunosuppression, diabetes and anatomical urinary tract obstructions e.g. urinary tract strictures, horseshoe kidneys, tumours, urinary calculi. Clinical presentation can consist of vague symptoms but may include constitutional symptoms of sepsis, flank pain, haematuria, dysuria and pyuria. A grossly nephrotic kidney may be palpable on palpation of the abdomen. Pyuria will be present on urinalysis. Radiological diagnosis can be made using CT investigations usually but also Ultrasound or MRI looking for evidence of urinary tract obstruction and pyelonephritis.Treatment will depend on the cause of the obstructing lesion. Emergent treatment involves drainage of the purulent build up within the kidney. This is performed by urology or interventional radiologists via percutaneous or retrograde ureteral stents to relieve the obstruction and drain the pus. Further surgical treatment will depend on the cause of obstruction. Antibiotic therapy is required for treatment of underlying infection or sepsis. If left untreated complications such as florid sepsis, xanthogranulomatous pyelonephritis, renal or perinephric abscess formation or fistula to pleura, colon or duodenum may occur.

336,77 €*

Menschliche Körperrepliken, um die Lehre zu verbessern!

Die bahnbrechende Anatomie Serie von Erler- Zimmer beinhaltet eine einzigartige und unerreichte Sammlung von kolorierten menschlichen Körperrepliken welche speziell entworfen wurden, um die Lehre und das Lernen zu verbessern. Diese Premiumkollektion von höchst akkurater humaner Anatomie wurde direkt aus radiologischen Daten oder echten Präparaten mit neuesten Bildgebenden Verfahren erzeugt. Die 3D menschliche Anatomie Serie bietet einen kosteneffektiven Weg, um Ihrem speziellen Unterrichts- und Demonstrationsbedarf im gesamten curricularen Bereich der Medizin, Gesundheitswissenschaften und der Biologie gerecht zu werden. Eine detaillierte Beschreibung der Anatomie, welche in jedem 3D-gedruckten Präparat dargestellt wird, wir mitgeliefert. Welche Vorteile bietet die Monash 3D Anatomie Serie im Vergleich zu Plastikmodellen oder echten menschlichen Plastinaten? Jede Körperreplik wurde sorgfältig entwickelt aus ausgewählten radiologischen Patientendaten oder präparierten menschlichen Körpern höchster Qualität, welche von einem hochqualifizierten Anatomenteam im Lehrzentrum für menschliche Anatomie der Monash Universität ausgewählt wurden, um klinisch wichtige Bereiche der Anatomie in einer Qualität und Detailtreue darzustellen, wie es mit konventionellen Modellen nicht möglich ist – es handelt sich um echte Anatomie, nicht um stilisierte. Jede Körperreplik wurde strengstens überprüft vom hochqualifizierten Anatomenteam im Lehrzentrum für menschliche Anatomie der Monash Universität, um die anatomische Genauigkeit des Endprodukts zu gewährleisten. Die Körperrepliken sind kein echtes menschliches Gewebe und unterliegen deshalb keinen Einschränkungen beim Transport, Import oder der Verwendung in Bildungseinrichtungen, die keine Erlaubnis zur Verwendung von Leichen haben. Die Die exklusive 3D Anatomie Serie vermeidet diese und andere ethische Probleme, welche auftreten, wenn man mit plastinierten menschlichen Überresten umgeht.

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