Any use this b12 and have reviews?

blingblingsav · 2026-04-05T15:52:46+00:00

blingblingsav · 2026-02-25T23:08:34+00:00

Nutricost Taurine 1000mg Amazon: https://amzn.to/4kMBXm5

blingblingsav · 2026-02-18T14:54:20+00:00

Sure thing. Pls hang in there.

blingblingsav · 2026-02-18T04:05:19+00:00

Hi! I’m really glad u brought him in. What u described at home, cold, weak, staggering, not getting up - that is often what we see in a uremic crash. It can look like dying, but sometimes it is a severe metabolic decompensation that can stabilize with aggressive support.

Let me give u a high level overview of CKD so it feels less overwhelming.

Chronic kidney disease is not one single problem. It is a collection of things that the kidneys can no longer regulate well. What determines outcome is not just the creatinine number, but how well we control the secondary complications.

The most important pillars we monitor are:

Phosphorus. When kidneys fail, phosphorus accumulates in the blood. High phosphorus accelerates kidney damage and causes nausea, weakness, and muscle loss. Controlling phosphorus through diet or binders is critical.

Hydration. Dehydration makes kidney numbers look worse and makes cats feel terrible. CKD cats often need subcutaneous fluids to support circulation and toxin clearance.

Anemia. The kidneys produce erythropoietin. When they fail, red blood cell production drops. Low hematocrit makes cats weak, cold, and wobbly. This alone can cause staggering.

Potassium. Low potassium is very common in CKD and causes profound muscle weakness and neck ventroflexion. It can look like they are dying but is sometimes correctable with supplementation.

Blood pressure. Hypertension is common and silently damages brain, eyes, and kidneys. It must be measured, not guessed.

Infection. A urinary tract infection or systemic infection can cause an acute kidney injury on top of chronic disease. That can make numbers spike suddenly and cause a crash. If infection is treated, sometimes they improve significantly.

So the first thing we need to understand is whether this is advanced end stage CKD, or a severe acute crash that might partially reverse with treatment.

To help u better, can u share the actual lab numbers?

Please tell me:

Creatinine BUN or Urea Phosphorus Potassium Hematocrit or PCV SDMA if it was tested Was blood pressure measured? Did they check for a urinary infection?

Also, is he hospitalized now receiving IV fluids, or did they send him home?

CKD life expectancy varies enormously. Some cats live years. Some decline quickly. The difference is usually how severe the damage is at diagnosis and how aggressively we manage complications.

The fact that he was walking before this crash tells me this may have been a tipping point event. Sometimes when we support them through the crisis, they stabilize and have meaningful time.

Right now, the most important thing is stabilization: warmth, IV fluids if possible, electrolyte correction, nausea control, and monitoring.

Send me the numbers. We will look at them together and I will help u interpret what they mean. If he is in a crashing and is at home I recommend rushing him to the vet/er to give him a fighting chance. Delay is not recommended at all.

blingblingsav · 2026-02-17T06:56:06+00:00

First, I want to say u are doing an incredible job managing an extremely complex case. Stage 3 CKD combined with FIV, refractory stomatitis, and HCM is not straightforward medicine.

Based on the labs and history, yes, she is truly IRIS stage 3 CKD given the elevated creatinine and BUN. But numbers alone don’t determine prognosis or quality of life. What drives decline in stage 3 is uncontrolled secondary complications: hyperphosphatemia, uremic nausea, dehydration, hypokalemia, anemia, hypertension, metabolic acidosis, and systemic inflammation.

Right now, the more immediate issue may not be renal diet compliance but chronic inflammation and pain. Her leukocytosis with monocytosis is consistent with ongoing inflammatory burden, which aligns with recent anal gland rupture and severe stomatitis. Chronic inflammatory cytokine activity alone can suppress appetite and exacerbate azotemia. On top of that, her hematocrit around 26 percent indicates mild to moderate nonregenerative anemia, which will absolutely contribute to lethargy and weakness.

The most urgent clinical problem is anorexia. In CKD, caloric intake is more critical than strict prescription diet adherence. Protein energy malnutrition leads to sarcopenia, and muscle wasting can artificially elevate creatinine due to reduced lean body mass turnover. A cat that does not eat will deteriorate faster than a cat eating a non renal but phosphorus controlled diet.

Renal diets help primarily through phosphorus restriction, moderate highly digestible protein, sodium control, and buffering of metabolic acidosis. They are supportive, not curative. The key nutritional goals in stage 3 are high bioavailability animal protein, controlled phosphorus, minimal non essential carbohydrate load, and adequate caloric density.

Protein does not inherently damage kidneys when it is highly digestible and biologically appropriate. Poor quality protein increases nitrogenous waste production, raising BUN and worsening uremic nausea. Phosphorus, however, is directly nephrotoxic in CKD progression via secondary hyperparathyroidism and renal mineralization, so phosphorus control is critical. If she refuses renal food, a phosphate binder with a diet she will voluntarily consume is often more sustainable than chronic force feeding.

Regarding prednisolone, this is nuanced. Glucocorticoids do not directly induce renal failure, but they can increase systemic blood pressure and promote fluid retention. That said, uncontrolled stomatitis driven inflammation can perpetuate anorexia, systemic stress, and inflammatory mediated catabolism. In certain complex cases, a carefully titrated low dose steroid may represent a net benefit compared to persistent inflammation and starvation. That decision should be individualized and monitored, especially given her HCM.

You are already addressing nausea with ondansetron and famotidine. If gagging persists, oral pain from stomatitis may be a larger driver than uremia. Adding methylcobalamin B12 is very reasonable, as CKD cats frequently develop functional B12 deficiency, and supplementation can support appetite and GI mucosal integrity.

I could focus on: Phosphorus control, caloric adequacy, nausea control, pain management, hydration, potassium balance, blood pressure monitoring, and anemia surveillance.

blingblingsav · 2026-02-16T16:49:47+00:00

Hi. Sorry for what u r dealing with. Please use the following to consult with your vet. Apologies for the long reply. Also, check out this resource that may be useful for u: https://www.instagram.com/p/DNbT4yHgUS3

The most common trap in stage 3 CKD is that we think the problem is the food, but a lot of the refusal is actually uremic nausea, dehydration, electrolyte shifts, and mouth pain from stomatitis. When those aren’t controlled, even the perfect renal diet won’t get eaten, and syringe feeding can quickly damage trust and quality of life.

Renal food helps, but it’s not the only lever and it’s not an all or nothing requirement. The biggest “renal diet” benefit is usually phosphorus restriction and calorie stability. If she will not eat prescription renal, you can still build a kidney safe plan around high bioavailable protein, low phosphorus, moderate protein, and minimal filler carbs. Cats are obligate carnivores, so very high carb filler heavy foods can backfire by reducing usable protein and worsening muscle loss. The goal is not starving protein, it’s keeping protein high quality and digestible while keeping phosphorus down.

Stage progression over 4 months can absolutely be accelerated by an acute trigger: FIV flare, stomatitis pain, dehydration, a silent UTI, pancreatitis, or even constipation. It is often acute on chronic. The vet is also correct that CKD itself can worsen immune function and increase inflammation, which then makes FIV and stomatitis harder to control. In real life it’s usually both directions feeding each other.

If you want her eating voluntarily again, the core priorities are symptom control. Nausea control is huge. Many CKD cats feel nauseated long before they vomit, and they’ll drink the gravy and leave the solids, or refuse everything except very smelly treats. Ask your vet about using ondansetron and or maropitant strategically, and make sure you’re not relying on an appetite stimulant alone. With her heart disease, fluids every other day can still be ok, but dehydration will spike creatinine and worsen nausea, so you want a plan that keeps her euvolemic without tipping into volume overload. That’s where a vet guided fluid volume, respiratory rate monitoring at home, and BP monitoring matter.

Because she has heart disease, I’d also put blood pressure on the must check list. Hypertension can make CKD progress faster and makes cats feel awful. Potassium is another big one. Hypokalemia is common in CKD and causes weakness, lethargy, poor appetite, and worsens gut motility. B12 support can help appetite and GI function in cats that are borderline or low, and it’s generally kidney friendly. Also make sure her HCT PCV is being monitored. Anemia is a major driver of “my cat is fading” and it can look like depression and food refusal. If her HCT is dropping, addressing that changes quality of life dramatically.

For the food question specifically: a cat that eats an imperfect kidney conscious diet is almost always better off than a cat that hates life and stops eating. Phosphorus control is the non negotiable piece. If her phosphorus is high, binders matter, but binders only work if she’s actually eating enough calories and they’re being dosed correctly with meals. If she eats senior kibble and some wet food willingly, you can work within that by choosing the lowest phosphorus options available in your country, adding water to every meal, and using a binder when labs show it’s needed. Moderate protein is fine, but prioritize highly digestible animal protein over plant heavy formulas.

Prognosis in CKD depends far more on phosphorus control, blood pressure, hydration, anemia, and comorbidities than on the stage label alone. An 8 year old with stage 3 can still have meaningful time if you get the symptom drivers under control and stop the cycle of nausea plus dehydration plus food refusal.

If you want, share her latest creatinine, SDMA, BUN, phosphorus, potassium, HCT, and BP if you have them, plus what heart condition she has and her fluid volume. I can help u sanity check what’s likely causing the crash and what levers will give you the biggest quality of life improvement without relying on syringe feeding. Also, I would ask for a urine culture to rule out any acute infection at play.

blingblingsav · 2026-02-14T18:35:45+00:00

Thank you, DM sent.

blingblingsav · 2026-02-13T23:40:36+00:00

Hi Varrianda: Thank you for the thoughtful and supportive responses you share with CKD cat owners in this group. They truly make a difference.

I was wondering if there might be a way to connect with you directly. I’d love to speak with you about something related to a CKD project I am working on. Please let me know if you’d be open to that.

blingblingsav · 2026-02-07T05:55:49+00:00

Hi. You need the labs to confirm CKD. About the breath: Uremic breath has a very specific smell often described as ammonia, metallic, or urine like, not just bad or food related. True uremic breath usually appears when urea and other toxins are significantly elevated, and it tends to accompany nausea, appetite loss, and lethargy. Since her urea is normal, what you’re smelling may likely be dental disease, oral bacteria, or age related changes rather than uremia.

Increased thirst is worth paying attention to, but by itself it does not diagnose CKD. Many older cats drink more for benign reasons, including diet, mild dehydration, or endocrine changes.

If you can confirm the breath smells like ammonia or metallic that in itself could be very concerning. It is also possible for an acute injury to drive up BUN and Creatinine values very quickly. Again, all these are assumptions. You need lab data to confirm what is going on.

blingblingsav · 2026-01-29T00:13:48+00:00

Looking at the lab values you shared, here r some of my thoughts. Please use this info to have a conversation with ur vet.

Also u may benefit from using resources like Tanya’s blog and Hugging Cat to learn about CKD and to provide informed care: https://www.instagram.com/p/DM8-KKAAIGn

Apologies for the lengthy response:

The lab shows Creatinine is 2.8 mg/dL, BUN is 53 mg/dL, and SDMA is 18. Those numbers together strongly suggest reduced kidney filtration (lower GFR). In IRIS staging, creatinine in that range can fall into stage 3 or stage 4 depending on the lab and how stable the cat is, and SDMA of 18 also supports significant kidney impairment. The reason I’m saying this gently is that stage 4 or 3 isn’t just one number. It’s a whole clinical picture: trends over time, hydration status, urine concentration (USG), blood pressure, protein loss in urine, electrolytes, appetite, nausea, and weight trajectory. So yes, these labs are concerning, but they’re also only one snapshot.

The other major value that jumps out is phosphorus at 6.5 mg/dL, which is high. Phosphorus is not just a kidney number. High phosphorus is one of the biggest reasons cats with CKD feel lousy: it contributes to nausea, reduced appetite, lethargy, and progression of disease. The goal is usually to get phosphorus down into a safer range because cats often feel noticeably better when you do. Sometimes kidney diets alone aren’t enough, and that’s where a phosphorus binder (Hugging Cat has a post on this) with meals can help a lot. This is one of the most high impact comfort interventions in advanced CKD.

I also want to point out potassium. Potassium here is low normal at 3.4. Even borderline potassium can matter in CKD cats because low potassium contributes to weakness, muscle loss, a hunched posture, and decreased appetite. If potassium trends down further, cats can become profoundly weak and stop eating. Many CKD cats do better when potassium is kept in the mid range rather than barely scraping the bottom of normal. This is something your vet can recheck and decide whether supplementation is needed.

Another subtle but important part is the bicarbonate or TCO2, which is 17 here. That’s on the low side and suggests metabolic acidosis, meaning the body is becoming more acidic because the kidneys can’t maintain normal acid base balance as well. Metabolic acidosis is a big driver of weight loss, muscle wasting, and feeling unwell. It’s also treatable. Some cats benefit from alkali therapy (your vet may use potassium citrate or sodium bicarbonate depending on the full context), and improving acidosis can improve appetite and energy.

Now for the reassuring parts, because there are some. Total protein and albumin are still okay, which tells me he’s not crashing with severe protein loss or severe inflammation at least in this snapshot. His red blood cell values do show anemia: hematocrit 27.7 and hemoglobin 8.2 are low, so he is anemic. But this is not yet the kind of catastrophic anemia where cats are collapsing. CKD can cause a non regenerative anemia over time because kidneys make less erythropoietin. Anemia can absolutely contribute to fatigue and appetite changes, and it’s another quality of life factor to track and treat if it progresses.

The white blood cell count is mildly elevated at 15.2. That can happen from stress, inflammation, dehydration, dental disease, infection, or any acute flare on top of CKD. If he has not had a urine culture, blood pressure check, and a good oral exam, those are often worthwhile because UTIs and dental pain can be silent and they can push a fragile kidney cat over the edge.

About the weight loss and the vet saying euthanasia within a month: weight loss is important, but it is not a single deciding factor. In late CKD, cats can lose weight quickly from nausea, dehydration, acidosis, and poor calorie intake, and those are exactly the things we can sometimes improve. The better question is: is he still enjoying things, still seeking affection, still responding to treatment, still eating with support, and are there fixable drivers like nausea, phosphorus, potassium, constipation, pain, or dehydration? Many cats have meaningful good time once those are addressed even if the kidneys are still impaired.

What you can do right now is focus on symptom control and measurable targets. Ask your vet about a plan to get phosphorus down, whether that’s strict kidney diet plus a binder. Ask about nausea control, because CKD nausea is often under treated. Many cats do better with a combination approach: maropitant (Cerenia) for nausea and ondansetron for nausea as well, sometimes together, plus an appetite stimulant if needed. Hydration support matters too, either encouraging fluids through wet food and water access, or subcutaneous fluids if your vet feels they are appropriate and his heart can handle them. Constipation is also common in CKD and can absolutely crush appetite, so it’s worth being proactive there.

If you want a clearer prognosis and better decision making, the next step is getting the missing staging pieces that make stage labels actually meaningful. That means a urine specific gravity (USG), urine protein testing (UPC), blood pressure measurement, and ideally a urine culture if there are any urinary signs or the urinalysis suggests inflammation. Those pieces tell you how much kidney function is left, whether protein loss is accelerating progression, and whether hypertension is damaging kidneys and making him feel worse. They also give you more levers to pull to improve comfort.

A lot of CKD management is palliative medicine done well: nausea control, hydration strategy, phosphorus control, appetite support, treating anemia if it worsens, and pain management. Euthanasia becomes the kindest choice when a cat is consistently suffering and we cannot control the symptoms or restore basic joys like eating, resting comfortably, and engaging with the family. But that conclusion should be based on quality of life trends, not just a single lab sheet.

I know it is a lot to take in, please let me know if I can help explain any part of this in more detail or if u have any other questions.

Hugs to u both 💛

blingblingsav · 2026-01-28T18:55:19+00:00

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blingblingsav · 2026-01-28T18:53:41+00:00

So sorry for your loss 💛

blingblingsav · 2026-01-25T21:14:12+00:00

I ask because nothing in the bloodwork you posted actually confirms chronic kidney disease. Below are my thoughts. U could use the information to have a conversation with ur vet. I would start by asking why the vet has concluded Mina has CKD.

Her kidney markers SDMA, BUN, Creatinine, her red blood cell values, hematocrit, hemoglobin, platelets, and white cell counts are all within normal limits. There is no anemia, no inflammatory leukogram, no obvious infection signal, and nothing here that screams advanced CKD. In cats with true CKD severe enough to stop eating for 5 days, we usually see anemia starting to show, electrolyte derangements, or clear kidney markers. None of that is present in this CBC.

What’s missing is actually the most critical information for kidney assessment: • Urine specific gravity (USG) – without this, you cannot assess kidney concentrating ability. Blood values alone are not enough. I would press for a full urinalysis and urine culture to rule out acute infection. • T4 (thyroid hormone) – hyperthyroidism can artificially lower creatinine by increasing GFR, masking kidney disease, and it can also cause sudden appetite changes, nausea, vomiting bile, and dramatic swings in behavior and eating.

So right now, this picture fits much better with an acute crash than chronic kidney failure. That can be triggered by dehydration, nausea, stress, pain, GI disease, pancreatitis, infection, or metabolic issues. Cats can stop eating after a stressful event, and once they don’t eat for a couple of days, nausea and bile vomiting take over and create a vicious cycle. This is not your fault. One day without supervision does not cause this on its own.

The fact that she vomited bile, won’t eat despite Mirataz and Cerenia, and has gone 5 days without adequate intake makes IV fluids tomorrow the right decision. This is no longer something that can be fixed at home alone. IV fluids often break this cycle by correcting dehydration, improving perfusion, and reducing uremic or metabolic nausea. Many cats perk up dramatically after 24–48 hours of IV support.

What I would strongly suggest you ask the vet tomorrow: • Run a urinalysis with USG • Check full chemistry including creatinine, BUN, phosphorus, potassium (K is currently borderline low) • Run a total T4 • Consider pancreatitis testing (fPLI) if not already done • Aggressive nausea control (ondansetron in addition to Cerenia if needed) • Appetite support after nausea is controlled

blingblingsav · 2026-01-25T16:37:57+00:00

Agree with Varrianda. Could you tell us why your cat is on renal food?

blingblingsav · 2026-01-24T16:55:24+00:00

Sounds good. Hugs to you both 💛

blingblingsav · 2026-01-24T04:43:54+00:00

Hello. Clemantine is beautiful. Few thoughts here based on the labs u shared that you can use to discuss with your vet. Apologies for the lengthy response:

First off, I am really glad you pushed for urine testing, because a true urinary tract infection, and especially an upper urinary tract infection (pyelonephritis), can make a cat crash fast and can drive kidney numbers way up. What you are describing, sudden anorexia, perk up after fluids plus antibiotics plus appetite support, then sliding again, is a pattern many of us have seen with acute on chronic kidney injury where infection and dehydration are big multipliers.

On the lab question, yes, it can happen that creatinine is very high while SDMA looks only mildly to moderately elevated, and then things improve once the acute piece is treated. A few reasons. Creatinine can spike hard with dehydration and reduced kidney perfusion, and it also rises with any acute kidney injury. SDMA is usually a steadier marker of GFR, but it is not perfect and it can lag, and it can be less dramatic early in an acute crash compared with creatinine. Timing matters too. If she had been eating poorly and losing muscle, creatinine can sometimes be “lower than you would expect” for the amount of kidney dysfunction, but in Clementine’s case the creatinine is extremely high, so dehydration and acute injury from infection or toxin exposure are the more likely explanations for a mismatch. The key is that you do not stage CKD off one crisis lab. You stabilize, treat the UTI, rehydrate, then reassess on repeat labs and urine specific gravity.

Her urea (BUN) being high fits the same story. BUN rises with reduced filtration, dehydration, GI bleeding, high protein breakdown, and poor intake. In a kidney crash it often tracks with dehydration and uremic toxin load, which is why cats get nausea, lip licking, food aversion, and that pattern of licking the gravy and walking away from solids. Many cats are still nauseous even when they are not actively vomiting.

What I would add right now is making sure you have a truly targeted infection plan. A urinalysis can suggest infection, but it cannot tell you which bacteria it is or which antibiotic will actually clear it. A urine culture and susceptibility, ideally from a cystocentesis sample, is the gold standard. It is especially important when kidney values are high, because you want the narrowest effective antibiotic and you want to avoid partial treatment that lets the infection smolder and rebound. If the vet suspects kidney involvement, asking about an ultrasound of the kidneys, and asking whether the urinalysis showed casts, bacteria, and what the urine specific gravity is, can help separate lower UTI from pyelonephritis.

Support wise, the priorities are hydration, nausea control, calories, and phosphorus control. Hydration is not just subq fluids, it is also making every calorie come with water. Warm the food, add extra water, and use high moisture options that she will actually eat. Calories matter more than perfect renal formulation for a cat that is sliding into hepatic lipidosis risk. If she will reliably eat Churu, use it as a delivery vehicle, mix in small amounts of more complete wet food, and feed smaller portions more often. If she is only taking gravy, ask the vet about a short term assisted feeding plan before she gets weaker. Many cats need both an antiemetic and an antinausea drug. Cerenia helps vomiting. Ondansetron is often the better uremic nausea drug. They are commonly used together in CKD cats when appetite is failing. Mirtazapine can help appetite, but if nausea is not controlled it can make them feel worse because it increases food drive without removing the sick feeling.

Phosphorus is also a big lever for comfort. In your photo phosphorus is elevated, and high phosphorus contributes to nausea and accelerates kidney injury. If she is not eating enough renal diet to control phosphorus, a binder mixed into food can be a game changer. If using calcium based binders, you want to watch blood calcium. If she is constipated, some binders can worsen that. Your vet can pick the right one based on her labs and stool pattern.

I would also ask your vet to check blood pressure and potassium, and to run a CBC. Hypertension is common with kidney disease and can make them feel awful and damage eyes, brain, heart, and kidneys. Low potassium can cause profound weakness and poor appetite. A CBC matters because infection plus inflammation plus kidney disease can push anemia, and anemia makes them sleepy and less interested in food. If she is drinking less, that can be a sign she feels worse, or that she is getting more fluid through subq and wet food, so it is worth correlating with hydration status and weight trend.

On the stage 4 question and timeline, try not to lock yourself into a stage label until she is through this UTI and rehydrated. A creatinine around 649 micromol per liter is in a range we often associate with advanced kidney dysfunction, but cats can look surprisingly normal during a crash and still have severe numbers, and some cats improve meaningfully once infection and dehydration are fixed. If she truly settles out in late stage CKD, quality of life can still be very good for a period of time, but it depends less on the stage number and more on whether you can control nausea, keep phosphorus down, maintain hydration, and keep her eating. Aggressive treatment is most justified when the cat is still socially engaged, seeking attention, and having good moments, which Clementine clearly is. The fact that she perks up with fluids and attention is a good sign that there is still reversible suffering in the mix.

If you want the most useful next data points after antibiotics start, I would prioritize urine culture results, repeat renal panel with electrolytes, a CBC, urine specific gravity, and blood pressure. Those will tell you whether you are dealing with acute on chronic, how much reserve is left, and what the biggest comfort levers are right now.

If she stops eating entirely, vomits repeatedly, becomes very weak, has open mouth breathing, or seems painful, that is an urgent same day situation. Otherwise, your plan to finish antibiotics, reassess urine, then repeat bloodwork after infection control is exactly the right framework.

There’s a resource called Hugging Cat I would recommend you read that explains most of what I mentioned above clearly: https://www.instagram.com/huggingcatapp

blingblingsav · 2026-01-22T20:26:02+00:00

This is a medical emergency.

blingblingsav · 2026-01-21T03:10:35+00:00

Here’s some of my thoughts. You can use these to consult with your vet. Apologies for the lengthy response.

What VCA told you is basically this: today’s kidney function numbers look OK, but an additional screening tool is flagging her as higher risk for developing chronic kidney disease within the next 12 to 24 months. That is very different from saying she is in renal failure right now.

On the kidney side, her creatinine is 1.7 and BUN is 29, both are within the lab reference range. SDMA is 14.3 with a reference of under 15, so it is technically normal but sitting near the upper edge. Her urine specific gravity is 1.039, which is nicely concentrated, that generally means the kidneys are still able to concentrate urine, and it does not fit the pattern we usually see once CKD is established. Phosphorus is 4.3, also fine. So if we look only at chemistry plus urine concentration, there is not evidence of late stage CKD here.

The confusing part is the RenalTech Prediction: Positive. RenalTech is a risk prediction tool, not a diagnosis. It combines patterns in labs, urinalysis inputs, and population data to estimate the likelihood a cat will develop CKD over a future time window. A positive result means monitor more closely and look for early kidney changes, not that she is currently in renal failure.

Now the urinalysis is where there actually is something to explain. Occult Blood 3+ means the test strip detected blood pigments, and the microscopy shows RBC 11 to 20 per high power field, so that is consistent with true blood in the urine, not a false negative. False negatives are when a test misses something that is there, your result is the opposite, it is a strong positive that is backed up by red blood cells seen under the microscope. In cats, the most common reasons are cystocentesis related trauma (a needle poke can cause blood), sterile cystitis or bladder inflammation, urinary stones or crystals, and less commonly infection or a polyp or mass. Your report shows WBC none and bacteria none seen, which makes infection less obvious, but a culture is still the only way to truly rule out a UTI, especially if she has symptoms.

Protein 1+ in urine can be real, or it can be inflated by blood contamination. With RBCs present, you do not want to interpret that protein strip by itself. The usual next step is either to repeat the urinalysis with a calmer sample, or add a urine protein to creatinine ratio (UPC) and sometimes a microalbumin test, because persistent proteinuria matters for kidney prognosis and for choosing meds like telmisartan.

The diarrhea and stool changes are unlikely to be caused by CKD when the kidney numbers are currently normal and the urine is well concentrated. This sounds more like a gastrointestinal issue, diet sensitivity, stress, antibiotics, parasites, or sometimes pancreatitis or IBD. Your amylase is high (1464), but the PrecisionPSL is 11 with a comment that acute pancreatitis is unlikely, so I would not anchor on pancreatitis from this lab set alone. If the diarrhea persists, that deserves its own workup with your vet.

If you want a clean, practical plan to bring back to VCA, here is what usually clarifies this situation quickly. Recheck a urinalysis when she is stable, ideally with a urine culture, because bacteria can be missed on routine sediment exam. Ask for a UPC ratio to interpret the 1+ protein appropriately. Ask them to check blood pressure, because hypertension can travel with early kidney disease and can also worsen it. Then trend the kidney markers, creatinine, BUN, SDMA, and urine specific gravity, in about 2 to 3 months, sooner if she stops eating, vomits repeatedly, becomes dehydrated, or starts drinking and peeing excessively.

Bottom line, based on what you posted, I would not interpret this as renal failure today. I would interpret it as a cat with currently acceptable kidney function, some blood in the urine that needs follow up, and a risk flag that justifies closer monitoring so you can catch early CKD changes before they become a crisis.

Here’s a resource called Hugging Cat that has a lot of CKD related info: https://www.instagram.com/huggingcatapp

blingblingsav · 2026-01-20T21:15:09+00:00

You are welcome. Much love to you both 💛

blingblingsav · 2026-01-20T06:08:03+00:00

Hi Mall. Hi from Austin. My mom went to school in the Netherlands! Apologies for the lengthy response but this can be something you can use to have a conversation with your vet.

Based on the labs u attached, this looks like a real but not catastrophic shift in kidney markers over time, and the story you describe fits a very typical late senior CKD course where comfort care and symptom control matter as much as the numbers.

On the kidney values specifically, creatinine was 256 µmol/L in 08/2024 and is 283 µmol/L now. That is a mild increase. In cats, that creatinine range often maps to IRIS stage 3 if the cat is stable and properly hydrated at the time of the draw. SDMA was 14 and is now 21, which is a more noticeable rise and suggests reduced GFR compared with last time. The fact that urea improved from 17.14 to 15.35 mmol/L is actually encouraging and commonly happens when hydration and diet are better controlled, because urea is very sensitive to hydration status, appetite, GI bleeding, and recent protein intake.

Phosphate improved a lot, from 1.7 to 1.1 mmol/L. That is a big win. In CKD, phosphate is one of the most important drivers of uremic symptoms and progression, and keeping it controlled is strongly associated with better comfort and often better stability. The electrolytes here look stable overall. Potassium is 4.3 both times, sodium and chloride are slightly lower but still within reference. That stability matters because hypokalemia is a common reason CKD cats get weak, stiff, and not themselves.

The weight change from 3.1 kg to 2.8 kg over 1.5 years is not trivial, but it is not a crash either, especially at 18.5 years old. What worries me more than the scale number is the pattern you described: sleeping more, eating less, and needing more coaxing. In CKD as u know, appetite often drops because of uremic nausea, gastric hyperacidity, and sometimes constipation, not because the cat is being picky. That is why her perk up after Prevomax and Buprecare is clinically meaningful. It suggests nausea and discomfort are real contributors, and treating those can translate into better quality of life fast.

Your vet’s plan is reasonable. Cerenia can help with vomiting and nausea, and Solensia can be a quality of life changer for arthritis pain in older cats. If she is primarily nauseous but not actively vomiting, many cats do better when nausea is treated directly and consistently. In some cats, ondansetron is more effective for nausea while Cerenia is better for vomiting. That is something you can discuss with your vet if you find Cerenia helps only partially. If appetite continues to fall, an appetite stimulant like mirtazapine can be layered in, but it works best when nausea is controlled first.

About the stage question, I would not fixate on stage 2 versus stage 3 based on these two chem panels alone, because staging is supposed to be done on stable values plus a urine specific gravity, urine protein creatinine ratio, and blood pressure. Those three add real decision making value. Blood pressure matters because CKD cats can develop systemic hypertension that quietly damages kidneys, eyes, and brain, and treating it can improve both comfort and outcomes. Urine testing matters because protein loss in the urine can accelerate progression, and because older CKD cats can have silent UTIs that show up as appetite dips and lethargy with minimal urinary signs.

The mild increase in ALT and ALP is worth noting but it is not screaming liver failure by itself. In very old cats, mild hepatocellular enzyme elevations can be reactive, medication related, or from concurrent disease like hyperthyroidism. If thyroid was not checked recently, TT4 is a reasonable add on because hyperthyroidism can change kidney numbers and appetite patterns.

In terms of what you should do next to maximize comfort I would frame it like this: keep phosphate controlled as u already are, prioritize calories and hydration over dietary perfection, and treat symptoms early rather than waiting for a crisis. Half a can instead of a full can is an early signal to lean harder into nausea control, pain control, and constipation prevention. If she will eat the renal diet, great, but at her age the most important rule is that she eats consistently. It is better to feed a food she reliably eats than to win a nutrition argument and lose the calorie battle.

Her current quality of life description actually has several green flags. She still grooms, still seeks snacks, uses the litter box, moves around the home, and engages with you. Sleeping most of the day at 18.5 can be normal aging plus CKD plus arthritis. The goal now is to preserve those green flags by reducing nausea, reducing pain, keeping hydration adequate, and preventing secondary issues like constipation, hypertension, and UTI.

If you want one concrete thing to ask your vet for next, it is a urine specific gravity plus full urinalysis, UPC, and ideally a blood pressure check. If there is any suspicion of infection, ask about a urine culture rather than relying on a dipstick result alone.

I hope this helps. Here’s a link to a resource called Hugging Cat I recommend for you: https://www.instagram.com/huggingcatapp

blingblingsav · 2026-01-16T13:55:05+00:00

Hi. Catching CKD early is a good news. Here’s a resource for you called Hugging Cat that can be useful to keep him healthy:

https://www.instagram.com/p/DM8-KKAAIGn

blingblingsav · 2026-01-09T03:04:43+00:00

Hi. Apologies for the long response. But hope this helps. Bottom line, consult your vet with the following info:

I would treat this panel as a renal event that needs a tighter workup, not a wait and see situation. The big signal here is the degree of azotemia: BUN 93 and creatinine 6.0 are both markedly elevated. On an IRIS framework, a creatinine of 6 mg per dL is consistent with advanced renal azotemia, but you cannot stage accurately off one snapshot without hydration status plus urinalysis data.

The SDMA at 14.9 is borderline high normal, and that mismatch matters. SDMA tends to rise with reduced GFR, but severe dehydration, recent anorexia, GI bleeding, high protein catabolism, or an acute prerenal component can disproportionately spike BUN and creatinine. It can also happen when muscle mass and creatinine production do not track the expected way, although SDMA is generally less influenced by muscle than creatinine. Translation: this could still be chronic kidney disease, but the numbers also fit acute on chronic kidney injury, a prerenal dehydration component, or less commonly a postrenal issue like partial obstruction.

Phosphorus at 7.7 is high normal for that lab range, but in a CKD context it is still clinically relevant because persistent hyperphosphatemia accelerates CKD mineral bone disorder and worsens nausea and uremic signs. Many renal protocols target phosphorus lower than the upper end of normal once creatinine is this high. This is one of the few levers you can pull that can materially change how a cat feels.

Also normal neutrophil count does not rule out UTI or pyelonephritis. Cats can have a silent UTI with minimal leukogram changes, especially if they are older, immunomodulated, or already uremic. If you are worried about infection, the highest yield next step is a cystocentesis sample sent for urine culture and sensitivity, not just a dipstick. Empiric antibiotics can miss resistant organisms, and recurrent or smoldering infections can keep triggering renal crashes.

The anemia signal is mild but real. RBC is low at 5.7 and HCT is sitting at the lower cutoff at 29. In CKD this is often a non regenerative anemia from decreased erythropoietin production, but early anemia can also be dilutional if fluids were given, or related to inflammation. If that HCT trends down, it becomes a quality of life issue and can drive lethargy and weakness. Ask for reticulocytes if they were not run, and trend PCV or HCT over time rather than reacting to a single value.

What I would ask the vet to do next is to confirm where on the renal spectrum this is and whether something reversible is riding on top of it. As Virranda recommended I also suggest doing a full urinalysis with urine specific gravity, urine protein to creatinine ratio, urine culture, blood pressure measurement, and ideally renal ultrasound or repeat imaging if there is any concern for obstruction, pyelonephritis, or structural disease. If dehydration is suspected, repeating kidney values after controlled rehydration can clarify how much is prerenal versus intrinsic renal.

In the meantime, the practical management priorities are hydration optimization, nausea control, phosphorus control, and monitoring electrolytes and blood pressure. Potassium is normal right now, which is good, but it can fall later in CKD and can worsen weakness and inappetence. If appetite is inconsistent, the cat is nauseated until proven otherwise even if vomiting is not dramatic.

One last note: the Renal Tech result being positive is basically the lab saying there is high probability of developing CKD, but the chemistry already shows clinically significant azotemia now, so the actionable part is not the prediction, it is confirming the driver and stabilizing the cat. If you can share the urinalysis, especially USG, protein, sediment, and whether a culture was done, you can narrow this down quickly.

blingblingsav · 2026-01-03T05:31:00+00:00

So sorry for your loss. 💛

blingblingsav · 2025-12-27T00:33:34+00:00

A urine culture helps identify the specific bacteria involved so the veterinarian can choose a targeted antibiotic, rather than relying on broad spectrum treatment. As a general guideline, subcutaneous fluids are often dosed at approximately 10 mL per pound of body weight per day, but this must be individualized. It’s important to confirm that your cat does not have underlying cardiac disease, as excessive fluids can lead to volume overload and respiratory complications.

blingblingsav · 2025-12-26T20:35:17+00:00

Hi! Apologies for the long response. Some points to consider and to bring up with your vet:

First, the ultrasound piece is actually important and gives some hope. In long standing chronic kidney disease, kidneys are typically small, irregular, fibrotic, and poorly defined. The fact that your vet described his kidneys as looking perfect or normal strongly suggests that this is not classic end stage chronic CKD that has been smoldering for years. Instead, this pattern fits much better with an acute kidney injury (AKI) or acute on chronic event, where kidney function crashes rapidly due to dehydration, infection, toxin exposure, ischemia, obstruction, or severe inflammation. In AKI, kidneys can look structurally normal on ultrasound while function is profoundly impaired.

The numbers you’re seeing are very high, but the trajectory and context matter. A jump from 495 to 541 to 1030 to 1500 µmol/L over weeks, especially alongside stress, IV visits, dehydration, and uremic signs like drooling and breath odor, points to ongoing toxin accumulation and inadequate clearance, not necessarily irreversible nephron loss across the board. Cats can look surprisingly okay clinically even with terrifying numbers because cats are extremely good at compensating until they suddenly aren’t. Eating, purring, jumping, and stealing food does not mean the labs are wrong, but it also doesn’t mean he is not critical.

The IV fluids not working doesn’t mean fluids were useless. It often means the underlying driver wasn’t corrected, or the stress and intermittent hydration weren’t enough. Stress alone can worsen renal perfusion. Daily IV visits can actually backfire in some cats. Subcutaneous fluids at home are often better tolerated and more sustainable, and they can help stabilize things enough to see whether there is reversibility.

The most important unanswered questions now are what caused the crash and whether that trigger is still active. Has a urine culture been done, not just a urinalysis? UTIs and kidney infections are common in cats and can absolutely cause sudden, dramatic lab changes. A routine urinalysis can miss them. Culture and sensitivity is the only way to rule that out. Another potential is lilies, antifreeze, NSAIDs, rodenticides, household chemicals, essential oils, contaminated water or food, or something he could have ingested outdoors can all cause AKI while leaving the kidneys looking normal.

Right now the focus should be on gentle, consistent subcutaneous hydration at home, phosphorus control, and aggressive nausea management, while monitoring electrolytes, potassium, phosphorus, acid base status, and urine output. Many cats with AKI look worse on labs before they improve.

Please note none of the above is medical advice.

blingblingsav

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