A Case of Pyelonephritis

A Case of Pyelonephritis: A Medical Student Clinical Pearl

Natasha Glover

MUN Medicine, CC4

Class of 2022

Reviewed by Dr. Paul VanHoutte

Copyedited by Dr. Mandy Peach

Case

Ms. X, a 23 year old mother of 2 presents to the Emergency Department with a 3 day history of left flank pain and vomiting. She describes the pain as sharp, constant, and worse with touch. Her boyfriend observed her sweating and shivering the night before. She has also experienced a loss of appetite, having been unable to keep any food or liquids “down”. In the ED waiting room, she vomits and describes bright red “streaks” mixed with the vomitus.

2 weeks prior to her visit, she describes having dysuria and suprapubic pressure. She has a history of frequent UTIs, so she took an old bottle of unfinished amoxicillin from a previous diagnosis of cystitis and took the remaining 3 pills over the course of the 3 days. Reports that dysuria and pressure subsided afterwards.

 

PMHx:
Frequent UTIs

 

Medications:
No prescription medications

 

Social:

Smokes marijuana daily

No EtOH consumption

No other recreational drug use

1 month ago became sexually active with a new partner, reports that partner was tested prior to beginning their sexual relationship

 

Physical Exam:

HR 112 BP 132/88 T 37.8 RR 18 SpO2 97%

Appears in mild discomfort. No respiratory distress. Oriented to person, place, and time. Dry oral mucosa. Skin tenting. No facial edema.

Mild tachycardia, otherwise normal cardiac exam. Equal breath sounds to the bases, no adventitious sounds. Abdomen was non-distended, soft, moderate tenderness in the LUQ and LLQ, no rebound tenderness, no masses, no evidence of hepatosplenomegaly. Tenderness at the left flank.

Peripheral pulses present, equal, capillary refill <2s . No peripheral edema.

 

Differential Diagnosis:

  1. Pyelonephritis
  2. Renal colic
  3. Ectopic pregnancy
  4. Gonorrhea/chlamydia infection
  5. Nephrotic syndrome
  6. Splenic flexure syndrome

 

Urinalysis:

Leukocyte esterase 25

Blood casts 50

Protein 20

HCG negative

Culture: E.coli positive (reported after 24 hours in lab)

 

Labs:

Sodium 140

Potassium 4.2

Chloride 108

Creatinine 274

Hgb 135

HCT 0.450
LKC 23.7

PLT 281

CRP 506.3

Lipase 8

Bedside renal U/S unable to detect any hydronephrosis.

A CT is ordered to rule out infected renal stone.

Left kidney is markedly larger than the right kidney. Stranding around the left kidney. No evidence of obstruction, hydronephrosis or hydroureter.

Assessment:

This patient is mildly hypovolemic. She also has a new AKI, likely pre-renal as the result of NSAID use and volume depletion. She has a left sided pyelonephritis given her recent history of cystitis (likely suboptimally treated by the use of old remaining antibiotics for a previous UTI), left flank pain with costovertebral tenderness and various abnormal lab findings

Imaging rules out obstructive causes and other complicating factors. As a result, she requires fluid resuscitation, pain management, nausea/vomiting management, IV antibiotics, and admission to the hospitalist unit.

 

Let’s Break it Down; Assessment of Acute Kidney Injury:

Pathogenesis of Pyelonephritis:

 

The majority of pyelonephritis cases are the result of lower genitourinary infections that travel up through the ureters and into the kidneys. Other sources of infection occur through hematogenous spread, which is most often seen in chronically ill and immunocompromised patients. Additionally, metastatic manifestations of fungal and staphylococcus may spread distantly from the skin. Escherichia coli is the most common pathogen observed in cases of pyelonephritis.

 

Treatment of pyelonephritis is highly dependent on whether or not it is classified as a complicated UTI or an uncomplicated UTI.

 

Complications:

 

-Higher mortality among elderly, immunocompromised patients, and those who develop septic shock

-A small number of individuals, particularly those with structural abnormalities, complex renal obstructions, congenital anomalies, develop chronic pyelonephritis. Chronic pyelonephritis is characterized by nonspecific symptoms as well as histologic findings of lymphoplasmacytic infiltrates, thyroidization, tubulointerstitial scarring, glomerulosclerosis, and fibrosis.  It accounts for approximately 20% of end-stage kidney disease.

Figure 2: Chronic pyelonephritis with focal and segmental glomerulosclerosis with periglomerular fibrosis (Jones silver stain) from the National Kidney Foundation

Management for Ms. X:

Ceftriaxone 1mg IV q24h because she was systemically unwell
Fluid resuscitation with normal saline
Pain management with acetaminophen 975 PO QID and morphine 5mg SC q3h PRN
Nausea and vomiting management with ondansetron (Zofran) 8mg IV q8h PRN
Admit to hospitalist for further monitoring and management

 

References:
1. Hooton, T., Gupta K. Acute complicated urinary tract infection (including pyelonephritis) in
adults. UpToDate. https://www.uptodate.com/contents/acute-complicated-urinary
-tract-infection-including-pyelonephritis-in-adults. Published 2021. Accessed July 14,
2021.
2. Buonaiuto VA, Marquez I, De Toro I, et al. Clinical and epidemiological features and
prognosis of complicated pyelonephritis: a prospective observational single
hospital-based study. BMC Infect Dis. 2014;14(1):639. doi:10.1186/s12879-014-0639-4
3. Fogo AB, Lusco MA, Najafian B, Alpers CE. AJKD Atlas of Renal Pathology: Chronic
Pyelonephritis. Am J Kidney Dis. 2016;68(4):e23-e25. doi:10.1053/j.ajkd.2016.08.001
4. Khanna R. Clinical presentation &amp; management of glomerular diseases: hematuria,
nephritic &amp; nephrotic syndrome. Mo Med. 2011;108(1):33-36.
http://www.ncbi.nlm.nih.gov/pubmed/21462608. Accessed July 14, 2021.
6. NB Provincial Health Authorities Anti-Infective Stewardship Committee. Treatment of adult
urinary tract infections. 2021. doi:10.1002/14651858.CD003237.pub2
7. Rahman M, Shad F, Smith MC. Acute kidney injury: A guide to diagnosis and management.
Am Fam Physician. 1970;86(7):631-639. https://www.aafp.org/afp/2012/1001/
p631.html. Accessed July 14, 2021.
8. Scheid DC. Diagnosis and Management of Acute Pyelonephritis in Adults. Vol 71.
American Academy of Family Physicians; 1970. https://www.aafp.org/afp/
2005/0301/p933.html. Accessed July 12, 2021.

 

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Acute Kidney Injury

Medical Student Clinical Pearl – January 2020

Carine Nzirorera

 

Faculty of Medicine
Dalhousie University
CC3
Class of 2021

Carine Nzirorera- ResearchGate

 

Reviewed and Edited by Dr. David Lewis

All case histories are illustrative and not based on any individual


 

Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function and is classified based on changes in serum creatinine level, reduction of urine output, and need for renal replacement therapy [1]. The Kidney Disease: Improving Global Outcomes (KDIGO) is the most preferred definition and staging system. According to KDIGO guidelines AKI is define as an 1) increase in serum creatinine by ≥0.3 mg/dL (≥26.5 µmol/L) within 48 hours, or 2) an increase in serum creatinine ≥ 1.5 fold from baseline within 7 days, or 3) urine output <0.5 mL/kg/hour for 6 hours [2].

KDIGO staging criteria [2]

Stage 1 an increase of serum creatinine level of 1.5 to 1.9 times baseline, OR increase in serum creatinine by ≥0.3mg/dL (≥26.5 µmol/L) OR a urine output less than 0.5 mL/kg/hour for 6 to 12 hours.

Stage 2 an increase of serum creatinine level of 2 to 2.9 times baseline OR a urine output less than 0.5 mL/kg/hour for more than 12 hours.

Stage 3 an increase of serum creatinine level of greater than 3 times baseline OR increase in serum creatinine to ≥4.0 mg/dL (≥353.6 µmol/L), OR a urine output less than 0.3 mL/kg/hour for ≥24 hours OR anuria output ≥12 hours OR initiation of renal replacement therapy such as dialysis.


 

Case Presentation

69y male with a history of kidney stones had experienced 1 week of hematuria, 1 month of bilateral flank pain and unintentional 20 lbs weight loss over 2 months. Patient was scheduled for a CT scan of his urinary tract and was urgently sent to emergency department after his creatinine levels were found to be severely elevated (2300 µmol/L).

Patient had a 20 year history of kidney stones and previous abdominal CT scans showed small stones in both kidneys =/< 2mm. Patient was afebrile, had no dysuria or increased frequency but complained of difficulty initiating urination and noticed a reduction of the stream even when his bladder felt full. Patient noted no vomiting, diarrhea or decrease in fluid and food intake. Patient had a positive family history of bladder cancer and was a smoker for 30+ years.


 

Etiology

Causes of acute kidney injury are organized based on located of the insult (Table 1) [1]. Causes related to decrease in renal perfusion are classified as prerenal injury. Decrease renal perfusion is seen in sepsis due to decreased arterial pressure from systemic vasodilation; intravascular volume depletion from vomiting, diarrhea or overuse of diuretics can also reduce circulation to the kidneys [1]. Lastly drugs like nonsteroidal anti-inflammatory drugs (NSAIDs) and angiotensin-converting enzyme (ACE) inhibitor can lower intraglomerular pressure causing reduced glomerular filtration rate. NSAIDs and calcineurin inhibitors constrict afferent (or preglomerular) arterioles while ACE inhibitors and angiotensin receptor blockers dilate efferent (or postglomerular) arterioles [3].

Direct renal damage to glomeruli, tubules, interstitium or vasculature are classified as Renal injury. Nephritides can be caused by infection (viral, bacterial, and fungal), medication (antibiotics, antivirals, protein pump inhibitors) toxins (ethylene glycol, aminoglycoside, rhabdomyolysis) or are secondary to conditions like hypertension, prolonged hypotension, lupus, diabetes mellitus and vasculitis.

Impaired drainage of urine distal to the kidneys due to obstruction of the urinary tract is classified as Postrenal cause of acute kidney injury.  Common causes of obstruction are kidney stones, injury, prostate, cervical or bladder cancer.

Previously 70% of community acquired cases of acute kidney injury are classified as prerenal causes [4], a more recent study found 55% of community acquired acute kidney injury were renal disease, 35% pre-renal disease and 10% were postrenal [5].

 


 

Clinical Presentation, History and Physical Exam

Clinical presentation of acute kidney injury varies with severity and varies with prerenal, renal and postrenal causes (Table 2). Patients with mild to moderate acute kidney injury are usually asymptomatic and identifiable by laboratory testing. Severe cases would present with vomiting, confusion, fatigue, anorexia, nausea, weight gain or edema [6]. Decline in mental status, asterixis or neurologic symptoms can be indicative of uremic encephalopathy, anemia or bleeding caused by uremic platelet dysfunction [1].

History and physical exam should determine cause of the kidney injury. Screening questions should be used to determine renal perfusion, any potential source of renal injury and any symptoms suggestive of obstructive uropathy (Table 2). Decreased renal perfusion can be assumed from a history of gastrointestinal illness, poor oral intake, use of diuretics, NSAIDs or ACE inhibitors [1,7]. Past medical history of diabetes mellitus, cardiac or liver disease can also indicate reduced renal perfusion [1,7]. Source of renal injury can be screen by assessing current medication for recent antibiotics, antiviral and protein pump inhibitors use, inquiring about past medical history of systemic illnesses such as lupus, viral, bacterial, or fungal infection or symptoms of infection such as rash, arthralgias, fatigue, and hematuria [1,7]. Postrenal cause can be determined from a history of gross hematuria, difficulty urinating, urgency or hesitancy to urinate or a history of kidney stones or bladder, prostate or cervical cancer [1,7].

 


 

Case continued

Blood work

  • CBC: elevated leukocytes (13.5) decreased erythrocytes (3.32), decreased hemoglobin (97), decreased Hematocrit (0.304) normal MCV
  • INR (1.2) APTT (44.3)
  • Liver function test were normal
  • Creatinine (2300)
  • Venous blood gas: decreased pH (7.17), decreased bicarbonate (13), pCO2 (36) and lactate (1.9 )
  • Electrolytes: elevated potassium (7.9), decreased sodium (131), decreased chloride (93), elevated glucose (10.7)

Figure 1. ECG of patient showing Sinus Rhythm and peaked T waves in V2, V3, and V4, an early manifestation of hyperkalemia. Other manifestations (not demonstrated here) include prolonged PR segment, loss of P wave, bizarre QRS complexes and sine wave.

 

PoCUS Imaging

Figure 2. Ultrasound imaging showing moderate hydronephrosis, areas of anechoic fluid indicated by red arrows.

CT Imaging

Figure 3. A) Pelvic CT showing bladder with diffuse wall thickening with a posterior globular neoplasm. B) Pelvic CT showing bladder with calculi within the neoplasm. C) Abdominal CT showing moderate bilateral hydronephrosis.

 

Diagnosis

It was determined that the cause of the acute kidney injury was diffuse thickening of the bladder wall causing obstruction of the ureterovesical junctions (Figure 3A and B). This resulted in bilateral moderate hydronephrosis (Figure 2 and 3C). Additionally, previous CBC reports showed the patient had chronic anemia likely from an underlying chronic kidney disease. This affected EPO production and resulted in decreased erythrocytes production from bone marrow.  With reduce erythrocytes, hemoglobin and hematocrit levels were also decreased. The acute kidney injury resulted in elevated creatinine level, leading to hyperkalemia and metabolic acidosis.

Management

Patient was admitted and fluid resuscitated. To correct his hyperkalemia patient was given 5 to 10 units of regular insulin and dextrose 50% intravenously to shift potassium out of circulation and into the cells. Calcium gluconate (10 mL of 10% solution infused over 5 mins) was given to reduce risk of arrhythmias.

To treat his bilateral hydronephrosis patient was sent to interventional radiology for placement of percutaneous nephrostomy tube. Follow up surgery will be needed to clear the ureters and biopsy of the bladder will be needed to determine treatment for the growth.  Depending on the remaining kidney function after treatment of the acute kidney injury the patient may require dialysis.


 

References

  1. Rahman, Mahboob, Fariha Shad, and Michael C. Smith. “Acute kidney injury: a guide to diagnosis and management.” American family physician 86.7 (2012): 631-639.
  2. KDIGO Clinical Practice Guideline for Acute Kidney Injury, Kidney Int Suppl. 2012;2(Suppl 1):8
  3. Erdbruegger Uta, Okausa Mark. “Etiology and diagnosis of prerenal disease and acute tubular necrosis in acute kidney injury in adults”. Uptodate (2019)
  4. Kaufman J, Dhakal M, Patel B, Hamburger R. Community-acquired acute renal failure. American Journal of Kidney Disease 2 (1991): 191–198.
  5. Obialo CI, Okonofua EC, Tayade AS, Riley LJ. Epidemiology of de novo acute renal failure in hospitalized African Americans: Comparing community‐acquired vs hospital‐acquired disease. Archives of Internal Medicine 160.9 (2000): 1309– 13.
  6. Meyer TW, Hostetter TH. Uremia. New England Journal of Medicine 357.13 (2007): 1316–1325.
  7. Mesropian, Paul Der, et al. “Community‐acquired acute kidney injury: A challenge and opportunity for primary care in kidney health.” Nephrology 21.9 (2016): 729-735.

 

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